Antirheumatic therapy is associated with reduced complement activation in rheumatoid arthritis
The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Theref...
Saved in:
| Published in | PloS one Vol. 17; no. 2; p. e0264628 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
25.02.2022
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1932-6203 1932-6203 |
| DOI | 10.1371/journal.pone.0264628 |
Cover
Loading…
| Abstract | The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers.
We assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment.
Median TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023).
Patients with active RA had elevated TCC, indicating increased complement activation. TCC decreased with antirheumatic treatment already after 6 weeks. However, only treatment with TNFi±MTX led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, possibly reflecting involvement of complement in the atherosclerotic process in RA. |
|---|---|
| AbstractList | The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers.
We assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment.
Median TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023).
Patients with active RA had elevated TCC, indicating increased complement activation. TCC decreased with antirheumatic treatment already after 6 weeks. However, only treatment with TNFi±MTX led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, possibly reflecting involvement of complement in the atherosclerotic process in RA. The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers. We assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment. Median TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023). The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers.BACKGROUNDThe complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers.We assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment.METHODSWe assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment.Median TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023).RESULTSMedian TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023).Patients with active RA had elevated TCC, indicating increased complement activation. TCC decreased with antirheumatic treatment already after 6 weeks. However, only treatment with TNFi±MTX led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, possibly reflecting involvement of complement in the atherosclerotic process in RA.CONCLUSIONSPatients with active RA had elevated TCC, indicating increased complement activation. TCC decreased with antirheumatic treatment already after 6 weeks. However, only treatment with TNFi±MTX led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, possibly reflecting involvement of complement in the atherosclerotic process in RA. Background The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers. Methods We assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment. Results Median TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023). Conclusions Patients with active RA had elevated TCC, indicating increased complement activation. TCC decreased with antirheumatic treatment already after 6 weeks. However, only treatment with TNFi±MTX led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, possibly reflecting involvement of complement in the atherosclerotic process in RA. Background The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers. Methods We assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment. Results Median TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023). Conclusions Patients with active RA had elevated TCC, indicating increased complement activation. TCC decreased with antirheumatic treatment already after 6 weeks. However, only treatment with TNFi±MTX led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, possibly reflecting involvement of complement in the atherosclerotic process in RA. BackgroundThe complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in rheumatoid arthritis (RA). The role of complement activation in response to treatment, and in development of premature CVD in RA, is limited. Therefore, we examined the effects of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation using soluble terminal complement complex (TCC) levels in RA; and assessed associations between TCC and inflammatory and cardiovascular biomarkers.MethodsWe assessed 64 RA patients starting with MTX monotherapy (n = 34) or TNFi with or without MTX co-medication (TNFi±MTX, n = 30). ELISA was used to measure TCC in EDTA plasma. The patients were examined at baseline, after 6 weeks and 6 months of treatment.ResultsMedian TCC was 1.10 CAU/mL, and 57 (89%) patients had TCC above the estimated upper reference limit (<0.70). Compared to baseline, TCC levels were significantly lower at 6-week visit (0.85 CAU/mL, p<0.0001), without significant differences between the two treatment regimens. Notably, sustained reduction in TCC was only achieved after 6 months on TNFi±MTX (0.80 CAU/mL, p = 0.006). Reductions in TCC after treatment were related to decreased C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and interleukin 6, and increased levels of total, high and low-density lipoprotein cholesterol. Similarly, baseline TCC was significantly related to baseline CRP, ESR and interleukin 6. Patients with endothelial dysfunction had higher baseline TCC than those without (median 1.4 versus 1.0 CAU/mL, p = 0.023).ConclusionsPatients with active RA had elevated TCC, indicating increased complement activation. TCC decreased with antirheumatic treatment already after 6 weeks. However, only treatment with TNFi±MTX led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, possibly reflecting involvement of complement in the atherosclerotic process in RA. |
| Audience | Academic |
| Author | Fagerland, Morten Wang Mikkelsen, Knut Eilertsen, Gro Ø. Agewall, Stefan Mollnes, Tom Eirik Hjeltnes, Gunnbjørg Feinberg, Mark W. Hokstad, Ingrid Nguyen, Thao H. P. Hollan, Ivana |
| AuthorAffiliation | 3 Department of Laboratory medicine, Innlandet Hospital Trust, Lillehammer, Norway 1 Lillehammer Hospital for Rheumatic Diseases, Lillehammer, Norway 7 Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway 2 University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Oslo, Norway 4 Oslo Centre for Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital, Oslo, Norway 16 Department of Cardiology, Oslo University Hospital, Ullevål, Oslo, Norway 13 Faculty of Health Sciences, Department of Clinical Medicine, UIT—The Arctic University of Norway, Tromsø, Norway 11 Division of Cardiology, Brigham and Women´s Hospital, Boston, Massachusetts, United States of America 15 Volvat Medical Center, Lillehammer, Norway Karolinska Institutet, SWEDEN 14 Department of Rheumatology, University Hospital of North Norway, Tromsø, Norway 8 Beitostølen Health and Sport Centre, Beitostølen, Norway 5 Department of Immunology, Osl |
| AuthorAffiliation_xml | – name: 14 Department of Rheumatology, University Hospital of North Norway, Tromsø, Norway – name: 8 Beitostølen Health and Sport Centre, Beitostølen, Norway – name: 16 Department of Cardiology, Oslo University Hospital, Ullevål, Oslo, Norway – name: 1 Lillehammer Hospital for Rheumatic Diseases, Lillehammer, Norway – name: 9 Norwegian University of Science and Technology, Gjøvik, Norway – name: 15 Volvat Medical Center, Lillehammer, Norway – name: 7 Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway – name: 5 Department of Immunology, Oslo University Hospital, Oslo, Norway – name: 13 Faculty of Health Sciences, Department of Clinical Medicine, UIT—The Arctic University of Norway, Tromsø, Norway – name: 3 Department of Laboratory medicine, Innlandet Hospital Trust, Lillehammer, Norway – name: 11 Division of Cardiology, Brigham and Women´s Hospital, Boston, Massachusetts, United States of America – name: 2 University of Oslo, Faculty of Medicine, Institute of Clinical Medicine, Oslo, Norway – name: 10 Harvard Medical School, Boston, Massachusetts, United States of America – name: 6 Research Laboratory, Nordland Hospital, Bodø, and Faculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway – name: 12 Department of Internal Medicine, Innlandet Hospital Trust, Lillehammer, Norway – name: 4 Oslo Centre for Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital, Oslo, Norway – name: Karolinska Institutet, SWEDEN |
| Author_xml | – sequence: 1 givenname: Thao H. P. orcidid: 0000-0003-2597-4031 surname: Nguyen fullname: Nguyen, Thao H. P. – sequence: 2 givenname: Ingrid surname: Hokstad fullname: Hokstad, Ingrid – sequence: 3 givenname: Morten Wang surname: Fagerland fullname: Fagerland, Morten Wang – sequence: 4 givenname: Tom Eirik surname: Mollnes fullname: Mollnes, Tom Eirik – sequence: 5 givenname: Ivana surname: Hollan fullname: Hollan, Ivana – sequence: 6 givenname: Mark W. surname: Feinberg fullname: Feinberg, Mark W. – sequence: 7 givenname: Gunnbjørg surname: Hjeltnes fullname: Hjeltnes, Gunnbjørg – sequence: 8 givenname: Gro Ø. surname: Eilertsen fullname: Eilertsen, Gro Ø. – sequence: 9 givenname: Knut surname: Mikkelsen fullname: Mikkelsen, Knut – sequence: 10 givenname: Stefan surname: Agewall fullname: Agewall, Stefan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35213675$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:149443623$$DView record from Swedish Publication Index |
| BookMark | eNqNU11v0zAUjdAQ2wr_AEEkJAQPLY7tOA4PSNXER6VJk_h6xHIcu_FI7GI7G_v3OG06mmlCyA9xrs85995j39PkyFgjk-RpBhYZKrI3l7Z3hreLTQwvACSYQPogOclKBOcEAnR0sD9OTr2_BCBHlJBHyTHKYYZIkZ8kP5YmaNfIvuNBizQ00vHNTap9yr23QvMg6_RahyZ1su5F_BG227SykyakXAR9FXnWpNqko4rVdcpdaJwO2j9OHireevlk_M6Sbx_efz37ND-_-Lg6W57PRZHjMK-UrAtAFYaEAlzUGAskiwwIRGtIVCkyUEghFKUVREAhQWoCVOwOZKSkuEaz5PlOd9Naz0ZrPIMEIYgpjRbMktUOUVt-yTZOd9zdMMs12wasW7NYtRatZIVCpKIwrwStMKGYFxBWgighYwVKqqg132n5a7npq4naGPoZd1EpJyUZcr8bq-urTtYieud4O6FNT4xu2NpeMUopKPPsb3vCaR-0YcY6zjIAUDH0iGlEvBpTOPurlz6wTnsh25YbafudEzQncOvEizvQ-_0aUWseLdFG2ViZGETZkpS4zAuYDWkX96DiqmWnRXyZSsf4hPB6QoiYIH-HNe-9Z6svn_8fe_F9in15gG0kb0PjbdsPj9NPgc8O7-L2EvYjEQF477X13kl1C8kAGyZvbxcbJo-Nkxdpb-_QhA7b2YiO6Pbf5D-sIDSm |
| CitedBy_id | crossref_primary_10_3389_fimmu_2023_1113015 crossref_primary_10_3390_jpm12101618 crossref_primary_10_1155_2024_1896817 crossref_primary_10_1021_acsnano_3c03828 crossref_primary_10_2147_OARRR_S318826 |
| Cites_doi | 10.1096/fj.00-0468fje 10.1038/s41584-018-0022-8 10.1136/annrheumdis-2019-216655 10.1016/j.amjmed.2008.06.014 10.1038/cr.2009.139 10.1016/j.thromres.2007.11.005 10.1152/ajplung.1991.260.4.L254 10.1016/j.molimm.2019.05.012 10.1016/j.ijcard.2014.04.057 10.1016/j.atherosclerosis.2015.05.038 10.1042/CS20180306 10.3390/cells10010148 10.1002/art.1780310302 10.1136/ard.2004.029124 10.1371/journal.pone.0174577 10.1016/j.semarthrit.2020.11.005 10.4049/jimmunol.1203487 10.1038/nrrheum.2015.40 10.1161/JAHA.114.001588 10.1002/art.10183 10.1136/annrheumdis-2011-200493 10.1038/nrrheum.2015.112 10.1093/ehjcvp/pvz033 10.1038/ni.2001 10.3109/03009742.2012.656698 10.1371/journal.pone.0253793 10.1016/j.molimm.2013.05.221 10.1016/S0735-1097(01)01746-6 10.1002/art.1780290603 10.1136/annrheumdis-2017-211735 10.1371/journal.pone.0169830 10.1007/BF02592409 10.1002/art.1780291108 10.1136/bmj.k1036 10.1136/annrheumdis-2011-200726 10.1177/039463201102400209 10.1186/s13075-017-1439-1 10.1097/BOR.0000000000000378 10.1038/cmi.2015.97 10.1172/JCI112721 10.1007/s102380200004 10.1016/j.freeradbiomed.2014.01.015 10.1038/nm.2538 10.1016/S0735-1097(00)00980-3 10.1002/art.1780341209 10.1371/journal.pone.0162316 10.1161/HYPERTENSIONAHA.118.11554 10.1016/j.molimm.2014.06.036 10.1136/ard.55.12.888 10.1101/cshperspect.a016295 10.1002/cbf.1745 10.1093/toxsci/kfm067 10.1371/journal.pone.0220079 10.1373/clinchem.2008.119214 10.3389/fimmu.2018.01057 10.1002/art.37916 10.1038/nri3345 10.1016/j.phanu.2013.07.001 10.1161/ATVBAHA.108.179705 10.1093/rheumatology/ken495 10.1016/j.autrev.2011.04.012 10.1016/S0735-1097(03)00329-2 10.1016/j.jacc.2004.08.062 10.1056/NEJMra1004965 10.4049/jimmunol.1403044 10.1111/j.1749-6632.1982.tb22140.x 10.1016/j.atherosclerosis.2016.11.015 10.1161/01.CIR.103.16.2084 10.1242/jcs.179291 |
| ContentType | Journal Article |
| Copyright | COPYRIGHT 2022 Public Library of Science 2022 Nguyen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. info:eu-repo/semantics/openAccess 2022 Nguyen et al 2022 Nguyen et al |
| Copyright_xml | – notice: COPYRIGHT 2022 Public Library of Science – notice: 2022 Nguyen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: info:eu-repo/semantics/openAccess – notice: 2022 Nguyen et al 2022 Nguyen et al |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM IOV ISR 3V. 7QG 7QL 7QO 7RV 7SN 7SS 7T5 7TG 7TM 7U9 7X2 7X7 7XB 88E 8AO 8C1 8FD 8FE 8FG 8FH 8FI 8FJ 8FK ABJCF ABUWG AEUYN AFKRA ARAPS ATCPS AZQEC BBNVY BENPR BGLVJ BHPHI C1K CCPQU D1I DWQXO FR3 FYUFA GHDGH GNUQQ H94 HCIFZ K9. KB. KB0 KL. L6V LK8 M0K M0S M1P M7N M7P M7S NAPCQ P5Z P62 P64 PATMY PDBOC PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS PTHSS PYCSY RC3 7X8 3HK 5PM ADTPV AOWAS D8T ZZAVC DOA |
| DOI | 10.1371/journal.pone.0264628 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Gale In Context: Opposing Viewpoints Gale In Context: Science ProQuest Central (Corporate) Animal Behavior Abstracts Bacteriology Abstracts (Microbiology B) Biotechnology Research Abstracts Nursing & Allied Health Database Ecology Abstracts Entomology Abstracts (Full archive) Immunology Abstracts Meteorological & Geoastrophysical Abstracts Nucleic Acids Abstracts Virology and AIDS Abstracts Agricultural Science Collection Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) ProQuest Pharma Collection Public Health Database (subscription) Technology Research Database ProQuest SciTech Collection ProQuest Technology Collection ProQuest Natural Science Collection ProQuest Hospital Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) Materials Science & Engineering Collection ProQuest Central (Alumni) ProQuest One Sustainability ProQuest Central UK/Ireland Advanced Technologies & Aerospace Collection Agricultural & Environmental Science Collection ProQuest Central Essentials Biological Science Collection ProQuest Central Technology collection Natural Science Collection Environmental Sciences and Pollution Management ProQuest One Community College ProQuest Materials Science Collection ProQuest Central Engineering Research Database Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student AIDS and Cancer Research Abstracts SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Materials Science Database (ProQuest) Nursing & Allied Health Database (Alumni Edition) Meteorological & Geoastrophysical Abstracts - Academic ProQuest Engineering Collection Biological Sciences Agriculture Science Database ProQuest Health & Medical Collection Medical Database Algology Mycology and Protozoology Abstracts (Microbiology C) Biological Science Database Engineering Database Nursing & Allied Health Premium Advanced Technologies & Aerospace Database ProQuest Advanced Technologies & Aerospace Collection Biotechnology and BioEngineering Abstracts Environmental Science Database Materials Science Collection ProQuest Central Premium ProQuest One Academic Publicly Available Content Database (subscription) ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China Engineering Collection Environmental Science Collection Genetics Abstracts MEDLINE - Academic NORA - Norwegian Open Research Archives PubMed Central (Full Participant titles) SwePub SwePub Articles SWEPUB Freely available online SwePub Articles full text DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Agricultural Science Database Publicly Available Content Database ProQuest Central Student ProQuest Advanced Technologies & Aerospace Collection ProQuest Central Essentials Nucleic Acids Abstracts SciTech Premium Collection ProQuest Central China Environmental Sciences and Pollution Management ProQuest One Applied & Life Sciences ProQuest One Sustainability Health Research Premium Collection Meteorological & Geoastrophysical Abstracts Natural Science Collection Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) Engineering Collection Advanced Technologies & Aerospace Collection Engineering Database Virology and AIDS Abstracts ProQuest Biological Science Collection ProQuest One Academic Eastern Edition Agricultural Science Collection ProQuest Hospital Collection ProQuest Technology Collection Health Research Premium Collection (Alumni) Biological Science Database Ecology Abstracts ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts Environmental Science Collection Entomology Abstracts Nursing & Allied Health Premium ProQuest Health & Medical Complete ProQuest One Academic UKI Edition Environmental Science Database ProQuest Nursing & Allied Health Source (Alumni) Engineering Research Database ProQuest One Academic Meteorological & Geoastrophysical Abstracts - Academic ProQuest One Academic (New) Technology Collection Technology Research Database ProQuest One Academic Middle East (New) Materials Science Collection ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Central ProQuest Health & Medical Research Collection Genetics Abstracts ProQuest Engineering Collection Biotechnology Research Abstracts Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Bacteriology Abstracts (Microbiology B) Algology Mycology and Protozoology Abstracts (Microbiology C) Agricultural & Environmental Science Collection AIDS and Cancer Research Abstracts Materials Science Database ProQuest Materials Science Collection ProQuest Public Health ProQuest Nursing & Allied Health Source ProQuest SciTech Collection Advanced Technologies & Aerospace Database ProQuest Medical Library Animal Behavior Abstracts Materials Science & Engineering Collection Immunology Abstracts ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic Agricultural Science Database |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 4 dbid: 8FG name: ProQuest Technology Collection url: https://search.proquest.com/technologycollection1 sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Sciences (General) Medicine |
| DocumentTitleAlternate | Impact of antirheumatic therapy on complement activation in rheumatoid arthritis |
| EISSN | 1932-6203 |
| ExternalDocumentID | 2633248820 oai_doaj_org_article_7f36b825bc8b4684a722bc6fcecf8fef oai_swepub_ki_se_756960 PMC8880951 10037_26348 A694957218 35213675 10_1371_journal_pone_0264628 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GeographicLocations | Norway United States--US Massachusetts |
| GeographicLocations_xml | – name: Norway – name: United States--US – name: Massachusetts |
| GrantInformation_xml | – fundername: ; – fundername: ; grantid: H2/2018 |
| GroupedDBID | --- 123 29O 2WC 53G 5VS 7RV 7X2 7X7 7XC 88E 8AO 8C1 8CJ 8FE 8FG 8FH 8FI 8FJ A8Z AAFWJ AAUCC AAWOE AAYXX ABDBF ABIVO ABJCF ABUWG ACGFO ACIHN ACIWK ACPRK ACUHS ADBBV AEAQA AENEX AEUYN AFKRA AFPKN AFRAH AHMBA ALIPV ALMA_UNASSIGNED_HOLDINGS AOIJS APEBS ARAPS ATCPS BAWUL BBNVY BCNDV BENPR BGLVJ BHPHI BKEYQ BPHCQ BVXVI BWKFM CCPQU CITATION CS3 D1I D1J D1K DIK DU5 E3Z EAP EAS EBD EMOBN ESX EX3 F5P FPL FYUFA GROUPED_DOAJ GX1 HCIFZ HH5 HMCUK HYE IAO IEA IGS IHR IHW INH INR IOV IPY ISE ISR ITC K6- KB. KQ8 L6V LK5 LK8 M0K M1P M48 M7P M7R M7S M~E NAPCQ O5R O5S OK1 OVT P2P P62 PATMY PDBOC PHGZM PHGZT PIMPY PQQKQ PROAC PSQYO PTHSS PV9 PYCSY RNS RPM RZL SV3 TR2 UKHRP WOQ WOW ~02 ~KM 3V. ADRAZ BBORY CGR CUY CVF ECM EIF IPNFZ NPM RIG PMFND 7QG 7QL 7QO 7SN 7SS 7T5 7TG 7TM 7U9 7XB 8FD 8FK AZQEC C1K DWQXO FR3 GNUQQ H94 K9. KL. M7N P64 PJZUB PKEHL PPXIY PQEST PQGLB PQUKI PRINS RC3 7X8 PUEGO 3HK AAPBV ABPTK N95 5PM ADTPV AOWAS D8T ZZAVC |
| ID | FETCH-LOGICAL-c754t-bfed708f4268047d44c3e710c38d26f9c107eccf88b230f3c6d60f932016984d3 |
| IEDL.DBID | BENPR |
| ISSN | 1932-6203 |
| IngestDate | Sun May 07 16:28:15 EDT 2023 Wed Aug 27 01:06:45 EDT 2025 Mon Sep 01 03:34:27 EDT 2025 Thu Aug 21 13:54:22 EDT 2025 Sat Apr 29 05:43:51 EDT 2023 Thu Sep 04 18:48:09 EDT 2025 Fri Jul 25 11:11:48 EDT 2025 Tue Jun 17 20:38:33 EDT 2025 Tue Jun 10 20:38:57 EDT 2025 Fri Jun 27 05:09:11 EDT 2025 Fri Jun 27 05:06:49 EDT 2025 Thu May 22 21:21:13 EDT 2025 Wed Feb 19 02:27:22 EST 2025 Tue Jul 01 03:53:59 EDT 2025 Thu Apr 24 23:10:05 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Language | English |
| License | This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Creative Commons Attribution License |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c754t-bfed708f4268047d44c3e710c38d26f9c107eccf88b230f3c6d60f932016984d3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 PLOS ONE Competing Interests: The authors have declared that no competing interests exist. We confirm that AbbVie does not alter our adherence to all PLOS ONE policies on sharing data and materials. |
| ORCID | 0000-0003-2597-4031 |
| OpenAccessLink | https://www.proquest.com/docview/2633248820?pq-origsite=%requestingapplication% |
| PMID | 35213675 |
| PQID | 2633248820 |
| PQPubID | 1436336 |
| PageCount | e0264628 |
| ParticipantIDs | plos_journals_2633248820 doaj_primary_oai_doaj_org_article_7f36b825bc8b4684a722bc6fcecf8fef swepub_primary_oai_swepub_ki_se_756960 pubmedcentral_primary_oai_pubmedcentral_nih_gov_8880951 cristin_nora_10037_26348 proquest_miscellaneous_2633856220 proquest_journals_2633248820 gale_infotracmisc_A694957218 gale_infotracacademiconefile_A694957218 gale_incontextgauss_ISR_A694957218 gale_incontextgauss_IOV_A694957218 gale_healthsolutions_A694957218 pubmed_primary_35213675 crossref_primary_10_1371_journal_pone_0264628 crossref_citationtrail_10_1371_journal_pone_0264628 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2022-02-25 |
| PublicationDateYYYYMMDD | 2022-02-25 |
| PublicationDate_xml | – month: 02 year: 2022 text: 2022-02-25 day: 25 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: San Francisco – name: San Francisco, CA USA |
| PublicationTitle | PloS one |
| PublicationTitleAlternate | PLoS One |
| PublicationYear | 2022 |
| Publisher | Public Library of Science Public Library of Science (PLoS) |
| Publisher_xml | – name: Public Library of Science – name: Public Library of Science (PLoS) |
| References | P. Libby (pone.0264628.ref004) 2008; 121 BR England (pone.0264628.ref001) 2018; 361 THP Nguyen (pone.0264628.ref031) 2021; 16 M Cutolo (pone.0264628.ref055) 2002; 20 L Wang (pone.0264628.ref076) 2014; 70 CS Crowson (pone.0264628.ref006) 2018; 77 F Corallini (pone.0264628.ref018) 2009; 48 EA Martin (pone.0264628.ref067) 2011; 29 TE Mollnes (pone.0264628.ref020) 1986; 29 KP Liao (pone.0264628.ref074) 2015; 4 G Hjeltnes (pone.0264628.ref029) 2013; 31 G Bergseth (pone.0264628.ref039) 2013; 56 A Tanaka (pone.0264628.ref037) 2018; 72 D Ricklin (pone.0264628.ref011) 2013; 190 pone.0264628.ref036 R Suresh (pone.0264628.ref059) 2016; 129 LM Title (pone.0264628.ref069) 2000; 36 DH Perlmutter (pone.0264628.ref047) 1986; 78 B. P. Morgan (pone.0264628.ref019) 1988; 73 M Holers (pone.0264628.ref013) 2018; 9 ETH Molenaar (pone.0264628.ref050) 2009; 48 M Galindo-Izquierdo (pone.0264628.ref012) 2021; 10 X Qin (pone.0264628.ref044) 2006; 3 I Navarro-Millán (pone.0264628.ref072) 2013; 65 EA Bemis (pone.0264628.ref017) 2019; 112 S Skeoch (pone.0264628.ref008) 2015; 11 KJ Shields (pone.0264628.ref028) 2017; 2 PO Bonetti (pone.0264628.ref038) 2004; 44 A Rozanski (pone.0264628.ref035) 2001; 103 A Familian (pone.0264628.ref042) 2005; 64 E Neumann (pone.0264628.ref014) 2002; 46 GS Belinsky (pone.0264628.ref056) 2007; 97 G Di Muzio (pone.0264628.ref043) 2011; 24 JS Smolen (pone.0264628.ref033) 2020; 79 YT Konttinen (pone.0264628.ref016) 1996; 55 TE Mollnes (pone.0264628.ref021) 1986; 29 N Niyonzima (pone.0264628.ref027) 2015; 195 GP Eng (pone.0264628.ref053) 2016; 11 PM Ridker (pone.0264628.ref054) 2009; 55 S Perissutti (pone.0264628.ref046) 1994; 24 E Myasoedova (pone.0264628.ref073) 2017; 29 PO Bonetti (pone.0264628.ref034) 2003; 41 F Corallini (pone.0264628.ref062) 2009; 48 E Ballanti (pone.0264628.ref041) 2011; 10 I McInnes (pone.0264628.ref048) 2011; 365 JE Volanakis (pone.0264628.ref049) 1982; 389 G Hjeltnes (pone.0264628.ref063) 2012; 41 SM Gordon (pone.0264628.ref075) 2017; 259 T Tanka (pone.0264628.ref052) 2014; 6 G Deyab (pone.0264628.ref064) 2017; 19 AL Pasqui (pone.0264628.ref070) 2002; 2 JP Brodeur (pone.0264628.ref015) 1991; 34 R Bordy (pone.0264628.ref009) 2018; 14 C Viedt (pone.0264628.ref060) 2000; 14 E Hertle (pone.0264628.ref061) 2014; 174 P. Libby (pone.0264628.ref057) 2012; 32 M Bäck (pone.0264628.ref058) 2019; 16 RA Robbins (pone.0264628.ref077) 1991; 260 C Weber (pone.0264628.ref026) 2011; 17 MC Corretti (pone.0264628.ref066) 2002; 39 A Hovland (pone.0264628.ref024) 2015; 241 J Deanfield (pone.0264628.ref065) 2005; 23 JE Pope (pone.0264628.ref051) 2021; 51 Z Zhou (pone.0264628.ref045) 2016; 13 CD Bo (pone.0264628.ref068) 2014; 2 MT Nurmohamed (pone.0264628.ref002) 2015; 11 G Deyab (pone.0264628.ref030); 12 GR Geovanini (pone.0264628.ref005) 2018; 132 I Hollan (pone.0264628.ref007) 2020; 6 JR Dunkelberger (pone.0264628.ref010) 2010; 20 W Yin (pone.0264628.ref078) 2008; 122 JA Avina-Zubieta (pone.0264628.ref003) 2012; 71 B Engelmann (pone.0264628.ref023) 2013; 13 KT Lappegård (pone.0264628.ref022) 2014; 61 C Charles-Schoeman (pone.0264628.ref071) 2012; 71 I Hokstad (pone.0264628.ref040) 2019; 14 FC Arnett (pone.0264628.ref032) 1988; 31 G Hansson (pone.0264628.ref025) 2011; 12 |
| References_xml | – volume: 20 start-page: S76 issue: 6 year: 2002 ident: pone.0264628.ref055 article-title: Methotrexate in psoriatic arthritis publication-title: Clin Exp Rheumatol – volume: 14 start-page: 2370 issue: 15 year: 2000 ident: pone.0264628.ref060 article-title: The terminal complement complex C5b-9 stimulates interleukin-6 production in human smooth-muscle cells through activation of transcription factors NF-κB and AP-1 publication-title: FASEB J doi: 10.1096/fj.00-0468fje – volume: 14 start-page: 404 year: 2018 ident: pone.0264628.ref009 article-title: Microvascular endothelial dysfunction in rheumatoid arthritis. publication-title: Nat Rev Rheumatol doi: 10.1038/s41584-018-0022-8 – volume: 79 start-page: 685 issue: 6 year: 2020 ident: pone.0264628.ref033 article-title: EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2019 update. publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2019-216655 – volume: 121 start-page: S21 issue: 10 year: 2008 ident: pone.0264628.ref004 article-title: Role of Inflammation in Atherosclerosis Associated with Rheumatoid Arthritis publication-title: Am. J. Med doi: 10.1016/j.amjmed.2008.06.014 – volume: 20 start-page: 34 year: 2010 ident: pone.0264628.ref010 article-title: Complement and its role in innate and adaptive immune responses publication-title: Cell Research doi: 10.1038/cr.2009.139 – volume: 122 start-page: 221 issue: 2 year: 2008 ident: pone.0264628.ref078 article-title: Regulated complement deposition on the surface of human endothelial cells: effect of tobacco smoke and shear stress publication-title: Thromb Res doi: 10.1016/j.thromres.2007.11.005 – volume: 260 start-page: L254 issue: 4 year: 1991 ident: pone.0264628.ref077 article-title: Complement activation by cigarette smoke publication-title: Am J Physiol Cell Mol Physiol doi: 10.1152/ajplung.1991.260.4.L254 – volume: 112 start-page: 256 year: 2019 ident: pone.0264628.ref017 article-title: Complement and its Environmental Determinants in the Progression of Human Rheumatoid Arthritis publication-title: Mol. Immunol doi: 10.1016/j.molimm.2019.05.012 – volume: 174 start-page: 400 issue: 2 year: 2014 ident: pone.0264628.ref061 article-title: Complement activation products C5a and sC5b-9 are associated with low-grade inflammation and endothelial dysfunction, but not with atherosclerosis in a cross-sectional analysis: The CODAM study. publication-title: Int. J. Cardiol doi: 10.1016/j.ijcard.2014.04.057 – volume: 241 start-page: 480 issue: 2 year: 2015 ident: pone.0264628.ref024 article-title: The complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosis publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2015.05.038 – volume: 132 start-page: 1243 issue: 12 year: 2018 ident: pone.0264628.ref005 article-title: Atherosclerosis and inflammation: overview and updates publication-title: Clin. Sci doi: 10.1042/CS20180306 – volume: 10 start-page: 148 issue: 1 year: 2021 ident: pone.0264628.ref012 article-title: Complement as a Therapeutic Target in Systemic Autoimmune Diseases. publication-title: Cells doi: 10.3390/cells10010148 – volume: 31 start-page: 315 issue: 3 year: 1988 ident: pone.0264628.ref032 article-title: The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. publication-title: Arthritis Rheum doi: 10.1002/art.1780310302 – volume: 64 start-page: 1003 year: 2005 ident: pone.0264628.ref042 article-title: Infliximab treatment reduces complement activation in patients with rheumatoid arthritis publication-title: Ann Rheum Dis doi: 10.1136/ard.2004.029124 – volume: 48 start-page: 293 year: 2009 ident: pone.0264628.ref050 article-title: Complement activation in patients with rheumatoid arthritis mediated in part by C-reactive protein publication-title: Rheumatol – volume: 2 start-page: e0174577 issue: 3 year: 2017 ident: pone.0264628.ref028 article-title: Plasma complement and vascular complement deposition in patients with coronary artery disease with and without inflammatory rheumatic diseases publication-title: PLoS ONE doi: 10.1371/journal.pone.0174577 – volume: 51 start-page: 219 issue: 1 year: 2021 ident: pone.0264628.ref051 article-title: C-reactive protein and implications in rheumatoid arthritis and associated comorbidities publication-title: Semin Arthritis Rheum doi: 10.1016/j.semarthrit.2020.11.005 – volume: 190 start-page: 3831 issue: 8 year: 2013 ident: pone.0264628.ref011 article-title: Complement in immune and inflammatory disorders: pathophysiological mechanisms publication-title: J Immunol doi: 10.4049/jimmunol.1203487 – volume: 11 start-page: 390 issue: 7 year: 2015 ident: pone.0264628.ref008 article-title: Atherosclerosis in rheumatoid arthritis: is it all about inflammation? publication-title: Nat Rev Rheumatol. doi: 10.1038/nrrheum.2015.40 – volume: 4 start-page: e001588 issue: 2 year: 2015 ident: pone.0264628.ref074 article-title: The association between reduction in inflammation and changes in lipoprotein levels and HDL cholesterol efflux capacity in rheumatoid arthritis publication-title: J Am Heart Assoc doi: 10.1161/JAHA.114.001588 – volume: 46 start-page: 934 issue: 4 year: 2002 ident: pone.0264628.ref014 article-title: Local Production of Complement Proteins in Rheumatoid Arthritis Synovium publication-title: Arthritis Rheum doi: 10.1002/art.10183 – volume: 71 start-page: 1157 year: 2012 ident: pone.0264628.ref071 article-title: Cholesterol efflux by high density lipoproteins is impaired in patients with active rheumatoid arthritis publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2011-200493 – volume: 11 start-page: 693 year: 2015 ident: pone.0264628.ref002 article-title: Cardiovascular comorbidity in rheumatic diseases. publication-title: Nat. Rev. Rheumatol doi: 10.1038/nrrheum.2015.112 – volume: 6 start-page: 104 issue: 2 year: 2020 ident: pone.0264628.ref007 article-title: Lipid management in rheumatoid arthritis: a position paper of the Working Group on Cardiovascular Pharmacotherapy of the European Society of Cardiology publication-title: Eur Heart J Cardiovasc Pharmacother doi: 10.1093/ehjcvp/pvz033 – ident: pone.0264628.ref036 – volume: 12 start-page: 204 year: 2011 ident: pone.0264628.ref025 article-title: The immune system in atherosclerosis publication-title: Nat Immunol doi: 10.1038/ni.2001 – volume: 31 start-page: 415 issue: 3 year: 2013 ident: pone.0264628.ref029 article-title: Serum levels of lipoprotein(a) and E-selectin are reduced in rheumatoid arthritis patients treated with methotrexate or methotrexate in combination with TNF-α-inhibitor. publication-title: Clin Exp Rheumatol – volume: 41 start-page: 240 issue: 3 year: 2012 ident: pone.0264628.ref063 article-title: Endothelial function improves within 6 weeks of treatment with methotrexate or methotrexate in combination with a TNF-α inhibitor in rheumatoid arthritis patients publication-title: Scand J Rheumatol doi: 10.3109/03009742.2012.656698 – volume: 3 start-page: 333 year: 2006 ident: pone.0264628.ref044 article-title: The complement system in liver diseases publication-title: Cell Mol Immunol – volume: 16 start-page: e0253793 issue: 6 year: 2021 ident: pone.0264628.ref031 article-title: Antirheumatic therapy is not associated with changes in circulating N-terminal pro-brain natriuretic peptide levels in patients with autoimmune arthritis publication-title: PLoS ONE doi: 10.1371/journal.pone.0253793 – volume: 56 start-page: 232 issue: 3 year: 2013 ident: pone.0264628.ref039 article-title: An international serum standard for application in assays to detect human complement activation products publication-title: Mol Immunol doi: 10.1016/j.molimm.2013.05.221 – volume: 39 start-page: 257 issue: 2 year: 2002 ident: pone.0264628.ref066 article-title: Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force publication-title: J Am Coll Cardiol doi: 10.1016/S0735-1097(01)01746-6 – volume: 29 start-page: 715 issue: 6 year: 1986 ident: pone.0264628.ref021 article-title: Complement activation in rheumatoid arthritis evaluated by C3dg and the terminal complement complex publication-title: Arthritis Rheum doi: 10.1002/art.1780290603 – volume: 77 start-page: 48 issue: 1 year: 2018 ident: pone.0264628.ref006 article-title: Impact of risk factors associated with cardiovascular outcomes in patients with rheumatoid arthritis publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2017-211735 – volume: 12 start-page: e0169830 issue: 2 ident: pone.0264628.ref030 article-title: Anti-rheumatic treatment is not associated with reduction of pentraxin 3 in rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis. publication-title: PLoS ONE doi: 10.1371/journal.pone.0169830 – volume: 24 start-page: 45 year: 1994 ident: pone.0264628.ref046 article-title: Effect of cytokines on the secretion of the fifth and eighth complement components by HepG2 cells publication-title: Int J Clin Lab Res doi: 10.1007/BF02592409 – volume: 29 start-page: 1359 issue: 11 year: 1986 ident: pone.0264628.ref020 article-title: Complement activation in synovial fluid and tissue from patients with juvenile rheumatoid arthritis publication-title: Arthritis Rheum doi: 10.1002/art.1780291108 – volume: 361 start-page: k1036 year: 2018 ident: pone.0264628.ref001 article-title: Increased cardiovascular risk in rheumatoid arthritis: mechanisms and implications publication-title: BMJ doi: 10.1136/bmj.k1036 – volume: 71 start-page: 1524 issue: 9 year: 2012 ident: pone.0264628.ref003 article-title: Risk of incident cardiovascular events in patients with rheumatoid arthritis: a meta-analysis of observational studies publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2011-200726 – volume: 24 start-page: 357 issue: 2 year: 2011 ident: pone.0264628.ref043 article-title: Complement system and rheumatoid arthritis: relationships with autobodies, serological, clinic features and anti-TNF treatment. publication-title: Int J Immunopathol Pharmacol doi: 10.1177/039463201102400209 – volume: 19 start-page: 232 issue: 1 year: 2017 ident: pone.0264628.ref064 article-title: Methotrexate and anti-tumor necrosis factor treatment improves endothelial function in patients with inflammatory arthritis. publication-title: Arthritis Res. Ther. doi: 10.1186/s13075-017-1439-1 – volume: 29 start-page: 277 issue: 3 year: 2017 ident: pone.0264628.ref073 article-title: Lipids and lipid changes with synthetic and biologic disease modifying antirheumatic drug therapy in rheumatoid arthritis: implications for cardiovascular risk. publication-title: Curr Opin Rheumatol doi: 10.1097/BOR.0000000000000378 – volume: 13 start-page: 301 year: 2016 ident: pone.0264628.ref045 article-title: Hepatocytes: a key cell type for innate immunity publication-title: Cell Mol Immunol doi: 10.1038/cmi.2015.97 – volume: 78 start-page: 1349 year: 1986 ident: pone.0264628.ref047 article-title: Cachectin/tumor necrosis factor regulates hepatic acute-phase gene expression publication-title: J Clin Invest doi: 10.1172/JCI112721 – volume: 2 start-page: 33 issue: 1 year: 2002 ident: pone.0264628.ref070 article-title: Relationship between serum complement and different lipid disorders publication-title: Clin Exp Med doi: 10.1007/s102380200004 – volume: 70 start-page: 155 year: 2014 ident: pone.0264628.ref076 article-title: Nrf2 Signaling Modulates Cigarette Smoke Induced Complement Activation in Retinal Pigmented Epithelial Cells. publication-title: Radic Biol Med doi: 10.1016/j.freeradbiomed.2014.01.015 – volume: 17 start-page: 1410 issue: 11 year: 2011 ident: pone.0264628.ref026 article-title: Atherosclerosis: current pathogenesis and therapeutic options publication-title: Nat Med doi: 10.1038/nm.2538 – volume: 36 start-page: 2185 issue: 7 year: 2000 ident: pone.0264628.ref069 article-title: Oral glucose loading acutely attenuates endothelium-dependent vasodilation in healthy adults without diabetes: an effect prevented by vitamins C and E publication-title: J Am Coll Cardiol doi: 10.1016/S0735-1097(00)00980-3 – volume: 34 start-page: 1531 issue: 12 year: 1991 ident: pone.0264628.ref015 article-title: Synovial fluid levels of complement SC5b-9 and fragment Bb are elevated in patients with rheumatoid arthritis publication-title: Arthritis Rheum doi: 10.1002/art.1780341209 – volume: 23 start-page: 7 issue: 1 year: 2005 ident: pone.0264628.ref065 article-title: Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension. publication-title: J Hypertens – volume: 11 start-page: e0162316 issue: 9 year: 2016 ident: pone.0264628.ref053 article-title: Anti-Drug Antibodies, Drug Levels, Interleukin-6 and Soluble TNF Receptors in Rheumatoid Arthritis Patients during the First 6 Months of Treatment with Adalimumab or Infliximab: A Descriptive Cohort Study. publication-title: PLoS One doi: 10.1371/journal.pone.0162316 – volume: 72 start-page: 1060 issue: 5 year: 2018 ident: pone.0264628.ref037 article-title: Physiological Diagnosis Criteria for Vascular Failure Committee.Physiological Diagnostic Criteria for Vascular Failure publication-title: Hypertension doi: 10.1161/HYPERTENSIONAHA.118.11554 – volume: 61 start-page: 126 issue: 2 year: 2014 ident: pone.0264628.ref022 article-title: A vital role for complement in heart disease publication-title: Mol Immunol doi: 10.1016/j.molimm.2014.06.036 – volume: 55 start-page: 888 issue: 12 year: 1996 ident: pone.0264628.ref016 article-title: Complement in acute and chronic arthritides: assessment of C3c, C9, and protectin (CD59) in synovial membrane. publication-title: Ann Rheum Dis doi: 10.1136/ard.55.12.888 – volume: 6 start-page: a016295 year: 2014 ident: pone.0264628.ref052 article-title: IL-6 in Inflammation, Immunity, and Disease. publication-title: Cold Spring Harb Perspect Biol doi: 10.1101/cshperspect.a016295 – volume: 29 start-page: 272 issue: 4 year: 2011 ident: pone.0264628.ref067 article-title: Comparing EndoPAT and BIOPAC measurement of vascular responses to mental stress publication-title: Cell Biochem Funct doi: 10.1002/cbf.1745 – volume: 97 start-page: 582 issue: 2 year: 2007 ident: pone.0264628.ref056 article-title: The Contribution of Methotrexate Exposure and Host Factors on Transcriptional Variance in Human Liver publication-title: Toxicol Sci doi: 10.1093/toxsci/kfm067 – volume: 14 start-page: e0220079 issue: 7 year: 2019 ident: pone.0264628.ref040 article-title: Tumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational study publication-title: PLoS ONE doi: 10.1371/journal.pone.0220079 – volume: 55 start-page: 209 issue: 2 year: 2009 ident: pone.0264628.ref054 article-title: C-Reactive Protein: Eighty Years from Discovery to Emergence as a Major Risk Marker for Cardiovascular Disease publication-title: Clin Chem doi: 10.1373/clinchem.2008.119214 – volume: 16 start-page: 389 year: 2019 ident: pone.0264628.ref058 article-title: Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities publication-title: Nat. Rev. Cardiol – volume: 9 start-page: 1057 year: 2018 ident: pone.0264628.ref013 article-title: Complement in the Initiation and Evolution of Rheumatoid Arthritis. publication-title: Front. Immunol doi: 10.3389/fimmu.2018.01057 – volume: 65 start-page: 1430 issue: 6 year: 2013 ident: pone.0264628.ref072 article-title: Changes in lipoproteins associated with methotrexate or combination therapy in early rheumatoid arthritis: results from the treatment of early rheumatoid arthritis trial publication-title: Arthritis Rheum doi: 10.1002/art.37916 – volume: 13 start-page: 34 issue: 1 year: 2013 ident: pone.0264628.ref023 article-title: Thrombosis as an intravascular effector of innate immunity publication-title: Nat Rev Immunol doi: 10.1038/nri3345 – volume: 2 start-page: 1 issue: 1 year: 2014 ident: pone.0264628.ref068 article-title: Acute cigarette smoking impairs microvascular function in young moderate smokers: A potential model for studying vasoactive properties of food bioactives. publication-title: PharmaNutrition doi: 10.1016/j.phanu.2013.07.001 – volume: 73 start-page: 473 issue: 3 year: 1988 ident: pone.0264628.ref019 article-title: Measurement of terminal complement complexes in rheumatoid arthritis publication-title: Clin. Exp. Immunol – volume: 32 start-page: 2045 issue: 9 year: 2012 ident: pone.0264628.ref057 article-title: History of Discovery: Inflammation in Atherosclerosis publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.108.179705 – volume: 48 start-page: 293 year: 2009 ident: pone.0264628.ref062 article-title: The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: implications in rheumatoid arthritis. publication-title: Rheumatology doi: 10.1093/rheumatology/ken495 – volume: 10 start-page: 617 issue: 10 year: 2011 ident: pone.0264628.ref041 article-title: Role of the complement system in rheumatoid arthritis and psoriatic arthritis: Relationship with anti-TNF inhibitors publication-title: Autoimmun. Rev doi: 10.1016/j.autrev.2011.04.012 – volume: 41 start-page: 1761 issue: 10 year: 2003 ident: pone.0264628.ref034 article-title: Enhanced external counterpulsation improves endothelial function in patients with symptomatic coronary artery disease publication-title: J Am Coll Cardiol doi: 10.1016/S0735-1097(03)00329-2 – volume: 44 start-page: 2137 issue: 11 year: 2004 ident: pone.0264628.ref038 article-title: Noninvasive identification of patients with early coronary atherosclerosis by assessment of digital reactive hyperemia publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2004.08.062 – volume: 365 start-page: 2205 issue: 23 year: 2011 ident: pone.0264628.ref048 article-title: The Pathogenesis of Rheumatoid Arthritis publication-title: N Engl J Med doi: 10.1056/NEJMra1004965 – volume: 48 start-page: 293 year: 2009 ident: pone.0264628.ref018 article-title: The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: implications in rheumatoid arthritis. publication-title: Rheumatology doi: 10.1093/rheumatology/ken495 – volume: 195 start-page: 257 issue: 1 year: 2015 ident: pone.0264628.ref027 article-title: Reconstituted High-Density Lipoprotein Attenuates Cholesterol Crystal-Induced Inflammatory Responses by Reducing Complement Activation publication-title: J Immunol doi: 10.4049/jimmunol.1403044 – volume: 389 start-page: 235 year: 1982 ident: pone.0264628.ref049 article-title: Complement activation by C-reactive protein complexes publication-title: Ann N Y Acad Sci doi: 10.1111/j.1749-6632.1982.tb22140.x – volume: 259 start-page: 104 year: 2017 ident: pone.0264628.ref075 article-title: High density lipoproteins are modulators of protease activity: Implications in inflammation, complement activation, and atherothrombosis publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2016.11.015 – volume: 103 start-page: 2084 year: 2001 ident: pone.0264628.ref035 article-title: Peripheral arterial responses to treadmill exercise among healthy subjects and atherosclerotic patients publication-title: Circulation doi: 10.1161/01.CIR.103.16.2084 – volume: 129 start-page: 1928 issue: 9 year: 2016 ident: pone.0264628.ref059 article-title: Complement-mediated ‘bystander’ damage initiates host NLRP3 inflammasome activation. publication-title: J Cell Sci doi: 10.1242/jcs.179291 |
| SSID | ssj0053866 |
| Score | 2.421265 |
| Snippet | The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis in... Background The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis... Background The complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis... BackgroundThe complement system plays an important role in pathophysiology of cardiovascular disease (CVD), and might be involved in accelerated atherogenesis... |
| SourceID | plos doaj swepub pubmedcentral cristin proquest gale pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | e0264628 |
| SubjectTerms | Analysis Antirheumatic agents Antirheumatic Agents - pharmacology Antirheumatic Agents - therapeutic use Arteriosclerosis Arthritis Arthritis, Rheumatoid - drug therapy Atherogenesis Atherosclerosis Autoimmune diseases Biology and Life Sciences Biomarkers Blood & organ donations Blood Sedimentation C-reactive protein C-Reactive Protein - analysis Cardiology Cardiovascular disease Cardiovascular diseases Care and treatment Cholesterol Cholesterol, HDL - blood Cholesterol, LDL - blood Clinical medicine Complement Complement activation Complement Activation - drug effects Complement Membrane Attack Complex - analysis Diagnosis Dosage and administration Drug Administration Schedule Drug Therapy, Combination Erythrocyte sedimentation rate Erythrocytes Ethylenediaminetetraacetic acids Female Health sciences Heart diseases Hospitals Humans Inflammation Interleukin Interleukin 6 Interleukin-6 - blood Laboratories Male Medicine Medicine and Health Sciences Methotrexate Methotrexate - pharmacology Methotrexate - therapeutic use Middle Aged Patients Prevention Reduction Rheumatoid arthritis Risk factors Treatment Outcome Tumor necrosis factor inhibitors Tumor Necrosis Factor Inhibitors - pharmacology Tumor Necrosis Factor Inhibitors - therapeutic use |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lj9MwELZQT1wQy6uFBQxCPA7ZbRK_eiyI1YIESMCiPWElftCIVVI17YF_z4ztRkSstBy4tfEkVeblb1zPZ0KeeVlwpyTLWMVNBvNtnSmO9HjCO4AbeW0qXIf88FGcnrH35_z8j6O-cE9YpAeOijuWvhQ1lDG1UTUTilWyKGojvHHGK-88Zl-Y8_bFVMzBEMVCpEa5UubHyS5H6651R1B1YEMmAF4T4qgdTUmBuX_Iz5P1RddfBj7_3kM5YhoNs9PJTXIjwUq6jK9zQK659hY5SIHb05eJXfrVbfJ92W6bzcrtAlcrjf1Xv2jT0ypZylmKq7N0g6yu8CXsOg-riBS7IOIaLm1amp7SNZaCHleBHukOOTt5-_XNaZYOWciM5Gyb1d5ZOVceZmo1Z9IyZkoHsMOUyhbCLwzUh2Bmr1QN1YovjbBi7gH1IY2LYra8SyYtqHVKaK5Uaa3MHZiduYotbMW5dTlgAGkXVs3INGlct-DfSJdcSl2IksFQuTeBNomcHM_IuNDhHzcJRUpUpEYT6mTCGcmGu9aRnOMK-ddo3UEWqbXDBXA4nRxOX-VwM_IYfUPHPtUhQeilWECxCQU1_MzTIIH0Gi3u3_lR7fpev_v07R-EvnweCb1IQr4DdZgq9UzAOyFt10jycCQJScKMhqfoyXut9Kh1gNJQXs3hzr13Xz78ZBjGh-KevNZ1uyijAD6jzL0YDINmAdYjFyCfETkKk5HqxyNtswrs5gpmFID9M_I8BtTolnTpJ3wCS3EB9ff9_2HUB-R6gX0tyFXAD8lku9m5h4A2t_WjkFh-Az5DgOw priority: 102 providerName: Directory of Open Access Journals – databaseName: Scholars Portal Journals: Open Access dbid: M48 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1Zj9MwELaWIiFeVuxyNLCAQYjjIVWbOLb7gFBBrBakggQU7RNW4mNbUSWlaSX23zPjuJEiyvGWxOOkncMzY3s-E_LEiSSzUrCY5ZmOwd8WscwQHo87C-HGqNA5zkNOP_CzGXt_np0fkN2ZrYGB9d7UDs-Tmq2Xg58_Ll-Bwb_0pzaI0a7TYFWVdgA5BZZbXiFXwTdx1PMpa9cVwLo5DwV0f-oJgbD29lV2XJVH9G_H7d5qWdX7gtLf91Z2EEi91zq9QQ5DuEknjX4ckQNbHpNr07CgfkyOgm3X9HkAoH5xk3yblJvFem63Hs6VNiVal3RR0zwI0xqKE7h0jcCvcOM3pvuJRoqFEs00L12UNLylWhgKOjr3CEq3yOz07Zc3Z3E4hyHWImObuHDWiKF04MzlkAnDmE4tRCY6lSbhbqwhhQRNcFIWkNC4VHPDhw4CQ0R6kcykt0mvBA73CR1JmRojRhY0g9mcjU2eZcaOIEwQZmxkRPqB-aoEE0BE5VSohKcMmtKdNJQO-OV4jMZS-UU5AXlMw1OF0lRBmhGJ216rBr_jH_SvUdAtLaJv-wfV-kIFY1bCpbyA1LrQsmBcslwkSaG50xaY4KyLyENUE9WUsrZjiJrwMeSjkHPDZx57CkTgKHGLz0W-rWv17uPX_yD6_KlD9CwQuQrYofNQVgH_CZG9OpQnHUoYR3SnuY9KveNKjVyHaBsysCH03Cn6_uZHbTO-FLftlbbaNjQSImykudPYRctZiPwRLjCLiOhYTIf13ZZyMfcA6BKcDmQGEXna2FanS3j0Ha5AUhmHFP3u33__PXI9waIWBCrITkhvs97a-xBqbooHfvT4BRdef8Q priority: 102 providerName: Scholars Portal |
| Title | Antirheumatic therapy is associated with reduced complement activation in rheumatoid arthritis |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/35213675 https://www.proquest.com/docview/2633248820 https://www.proquest.com/docview/2633856220 http://hdl.handle.net/10037/26348 https://pubmed.ncbi.nlm.nih.gov/PMC8880951 http://kipublications.ki.se/Default.aspx?queryparsed=id:149443623 https://doaj.org/article/7f36b825bc8b4684a722bc6fcecf8fef http://dx.doi.org/10.1371/journal.pone.0264628 |
| Volume | 17 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3db9MwELdYJyFeEBsfLYxiEOLjIVuTOLb7hLppYyB1oMFQn2Yl_lgrpqQ07QP_PXeOWxQxAS9RG1-S9r58d_H9TMhLJ5LMSsEilmc6gvm2iGSG8HjcWQg34kLnWIccn_HTC_Zxkk1Cwa0OyyrXPtE7alNprJEfJDyFuR_iwcG7-Y8Id43Ct6thC40tsg0uWGYdsn14fPb5fO2LwZo5Dw1zqYgPgnz251Vp9yH7wMZMCHy1t6eyNTV5BP-Nn-7Mr6v6piD0z7WULcRRP0ud3CN3Q3hJR40-7JBbttwlt8fhBfou2Qm2XNM3AXD67X1yOSqXs8XUrjx8K21asn7SWU3zIDxrKBZs6QKBXuGLX4juC4sUGyOasi6dlTTcpZoZCjo59YhJD8jFyfHXo9Mo7LsQaZGxZVQ4a8RAOpi85YAJw5hOLUQiOpUm4W6oIWUEyTspC0hgXKq54QMHgSAiu0hm0oekUwKHu4TGUqbGiNiCJjCbs6HJs8zYGMICYYZG9kg3MF-VoPKIoJwKBbJmMJSupaF0wCvHbTOulX8JJyBvaXiqUJoqSLNHos1V8wav4x_0hyjoDS2ibfsT1eJKBeNVwqW8gFS60LJgXLJcJEmhudMWmOCs65FnqCaqaV3d-Aw14kPIPyHHhse88BSIuFHikp6rfFXX6sOnb_9B9OW8RfQ6ELkK2KHz0EYB_wmRvFqUey1K8Bu6NdxFpV5zpVa_LQyuXCv6zcPPN8N4U1ymV9pq1dBIiKiR5lFjFxvOQqSP8IBZj4iWxbRY3x4pZ1MPeC5hkoFMoEdeNbbVuiSc-g6fQFIZh5T88d9__xNyJ8EmFgQmyPZIZ7lY2acQWi6LPtkSEwFHeRTj8eR9P3iUvi_WwHHM5C-PCX-v |
| linkProvider | ProQuest |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1bb9MwFLbGkIAXxMZlhcEM4vqQrU0c231AqFzGxi5IY0N7wiS-rBVTUppWaH-K38g5jlMUMQEve2vjk7Q592P7fCbksRNxaqVgEctSHUG8zSOZIjwedxbSjV6uM5yH3NvnW0fsw3F6vEB-Nr0wuK2y8YneUZtS4xz5RswTiP2QD3Zfjb9HeGoUrq42R2jUarFjz35AyVa93H4L8n0Sx5vvDt9sReFUgUiLlE2j3FkjutJBaJJdJgxjOrEQZ3UiTcxdX0NBBO_lpMwhPXeJ5oZ3HaQ5iFsimUnguZfIZZYkfcTql5vvG88PvoPz0J6XiN5G0Ib1cVnYdah1sA0U0mztrbdoBUJ_XsA8KiyOT8vqvJT3z52bLXxTHxM3b5DrIZmlg1r7lsiCLZbJlb2wXL9MloLnqOjzAG_94ib5Miimo8nQzjxYLK0bwM7oqKJZUBVrKE4P0wnCysIXv-3dT2NSbMOoJ5HpqKDhKeXIULCAocdnukWOLkQet8liARxeIbQnZWKM6FnQO2Yz1jdZmhrbgyREmL6RHbISmK8KMDDEa06EAs1iMJQ00lA6oKPjIR2nyi_5CaiSap4qlKYK0uyQaH7XuEYH-Qf9axT0nBaxvf2FcnKigqtQwiU8h8I91zJnXLJMxHGuudMWmOCs65A1VBNVN8rOPZQa8D5Uu1DRw8888hSI71HgBqKTbFZVavvj5_8g-nTQInoWiFwJ7NBZaNqAd0LcsBblaosSvJRuDa-gUjdcqdRve4Y7G0U_f_jhfBgfipsCC1vOahoJ-TvS3KntYs5ZqCsQjDDtENGymBbr2yPFaOjh1SWENKg7OuRpbVutW8Klb_AJJJXyPu_e_fv_XyNXtw73dtXu9v7OPXItxvYZhERIV8nidDKz9yGpneYPvCeh5OtFu65fJrO16g |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1bb9MwFLZGJ028IDYuLQxmENeHbG3i2O4DQh3btDI2po2hPWESX7aKKSlNK7S_xq_jnMQpipiAl7218UnanPuxfT4T8syJMLZSsIAlsQ4g3qaBjBEejzsL6UYv1QnOQ-4f8N0T9v40Pl0gP-teGNxWWfvE0lGbXOMc-UbII4j9kA92N5zfFnG4tfN2_D3AE6RwpbU-TqNSkT17-QPKt-LNcAtk_TwMd7Y_vdsN_AkDgRYxmwaps0Z0pYMwJbtMGMZ0ZCHm6kiakLu-huII3tFJmUKq7iLNDe86SHkQw0QyE8Fzb5BFAVFRtsji5vbB4VEdB8CTcO6b9SLR2_C6sT7OM7sOlQ82hULSrUtbzhphsTw9YB4jWuOLvLgqAf5zH2cD7bSMkDu3yS2f2tJBpYvLZMFmK2Rp3y_er5Bl70cK-sqDXb--Q74Msulocm5nJXQsrdrBLumooIlXHGsoThbTCYLMwpdyE3w5qUmxKaOaUqajjPqn5CNDwR7OS7Smu-TkWiRyj7Qy4HCb0J6UkTGiZ0ELmU1Y3yRxbGwPUhJh-kZ2SNszX2VgbojeHAkFesZgKKqlobTHSscjOy5UuQAooGaqeKpQmspLs0OC-V3jCivkH_SbKOg5LSJ9lxfyyZnyjkMJF_EUyvhUy5RxyRIRhqnmTltggrOuQ9ZQTVTVNjv3V2rA-1D7Qn0PP_O0pEC0jwzt5iyZFYUafvz8H0THRw2il57I5cAOnfgWDngnRBFrUK42KMFn6cZwG5W65kqhfls33Fkr-tXDT-bD-FDcIpjZfFbRSMjmkeZ-ZRdzzkKVgdCEcYeIhsU0WN8cyUbnJdi6hAAHVUiHvKhsq3GLv_QNPoGkYt7n3Qd___9rZAnclvowPNh7SG6G2EuD-AjxKmlNJzP7CDLcafrYuxJKvl639_oFEX27hQ |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Antirheumatic+therapy+is+associated+with+reduced+complement+activation+in+rheumatoid+arthritis&rft.jtitle=PloS+one&rft.au=Nguyen%2C+Thao+H+P&rft.au=Hokstad%2C+Ingrid&rft.au=Morten+Wang+Fagerland&rft.au=Mollnes%2C+Tom+Eirik&rft.date=2022-02-25&rft.pub=Public+Library+of+Science&rft.eissn=1932-6203&rft.volume=17&rft.issue=2&rft.spage=e0264628&rft_id=info:doi/10.1371%2Fjournal.pone.0264628&rft.externalDBID=HAS_PDF_LINK |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1932-6203&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1932-6203&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1932-6203&client=summon |