Multiple cytokines and chemokines are associated with rheumatoid arthritis-related autoimmunity in first-degree relatives without rheumatoid arthritis: Studies of the Aetiology of Rheumatoid Arthritis (SERA)
Objective We investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree relatives (FDRs) of RA probands, a population without RA but at increased risk for its future development. Methods We studied 44 autoa...
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| Published in | Annals of the rheumatic diseases Vol. 72; no. 6; pp. 901 - 907 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BMJ Publishing Group Ltd and European League Against Rheumatism
01.06.2013
BMJ Publishing Group LTD |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Objective We investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree relatives (FDRs) of RA probands, a population without RA but at increased risk for its future development. Methods We studied 44 autoantibody positive FDRs, of whom 29 were rheumatoid factor (RF) positive, 25 were positive for the high risk autoantibody profile (HRP), that is, positive for anti-cyclic citrullinated peptide and/or for at least two RF IgM, IgG or IgA isotypes, and nine FDRs who were positive for both; and 62 FDRs who were never autoantibody positive. Twenty-five cytokines/chemokines were measured using a bead-based assay in serum. As a comprehensive measure of inflammation, we calculated a Cytokine Score by summing all cytokine/chemokine levels, weighted by their regression coefficients for RA-autoantibody association. We compared C-reactive protein, individual cytokines/chemokines and Cytokine Score to the outcomes: positivity for RF and for the HRP using logistic regression. Results Adjusting for age, sex, ethnicity and ever smoking, the Cytokine Score and levels of IL-6 and IL-9 were associated with both RF and HRP. IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon (IFN)-γ were associated with HRP only. Associations between the Cytokine Score and RF and HRP positivity were replicated in an independent military personnel cohort. Conclusions In first-degree relatives of patients with RA, RA-related autoimmunity is associated with inflammation, as evidenced by associations with multiple cytokines and chemokines. |
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| AbstractList | ObjectiveWe investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree relatives (FDRs) of RA probands, a population without RA but at increased risk for its future development.MethodsWe studied 44 autoantibody positive FDRs, of whom 29 were rheumatoid factor (RF) positive, 25 were positive for the high risk autoantibody profile (HRP), that is, positive for anti-cyclic citrullinated peptide and/or for at least two RF IgM, IgG or IgA isotypes, and nine FDRs who were positive for both; and 62 FDRs who were never autoantibody positive. Twenty-five cytokines/chemokines were measured using a bead-based assay in serum. As a comprehensive measure of inflammation, we calculated a Cytokine Score by summing all cytokine/chemokine levels, weighted by their regression coefficients for RA-autoantibody association. We compared C-reactive protein, individual cytokines/chemokines and Cytokine Score to the outcomes: positivity for RF and for the HRP using logistic regression.ResultsAdjusting for age, sex, ethnicity and ever smoking, the Cytokine Score and levels of IL-6 and IL-9 were associated with both RF and HRP. IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon (IFN)- gamma were associated with HRP only. Associations between the Cytokine Score and RF and HRP positivity were replicated in an independent military personnel cohort.ConclusionsIn first-degree relatives of patients with RA, RA-related autoimmunity is associated with inflammation, as evidenced by associations with multiple cytokines and chemokines. We investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree relatives (FDRs) of RA probands, a population without RA but at increased risk for its future development. We studied 44 autoantibody positive FDRs, of whom 29 were rheumatoid factor (RF) positive, 25 were positive for the high risk autoantibody profile (HRP), that is, positive for anti-cyclic citrullinated peptide and/or for at least two RF IgM, IgG or IgA isotypes, and nine FDRs who were positive for both; and 62 FDRs who were never autoantibody positive. Twenty-five cytokines/chemokines were measured using a bead-based assay in serum. As a comprehensive measure of inflammation, we calculated a Cytokine Score by summing all cytokine/chemokine levels, weighted by their regression coefficients for RA-autoantibody association. We compared C-reactive protein, individual cytokines/chemokines and Cytokine Score to the outcomes: positivity for RF and for the HRP using logistic regression. Adjusting for age, sex, ethnicity and ever smoking, the Cytokine Score and levels of IL-6 and IL-9 were associated with both RF and HRP. IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon (IFN)-γ were associated with HRP only. Associations between the Cytokine Score and RF and HRP positivity were replicated in an independent military personnel cohort. In first-degree relatives of patients with RA, RA-related autoimmunity is associated with inflammation, as evidenced by associations with multiple cytokines and chemokines. OBJECTIVEWe investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree relatives (FDRs) of RA probands, a population without RA but at increased risk for its future development.METHODSWe studied 44 autoantibody positive FDRs, of whom 29 were rheumatoid factor (RF) positive, 25 were positive for the high risk autoantibody profile (HRP), that is, positive for anti-cyclic citrullinated peptide and/or for at least two RF IgM, IgG or IgA isotypes, and nine FDRs who were positive for both; and 62 FDRs who were never autoantibody positive. Twenty-five cytokines/chemokines were measured using a bead-based assay in serum. As a comprehensive measure of inflammation, we calculated a Cytokine Score by summing all cytokine/chemokine levels, weighted by their regression coefficients for RA-autoantibody association. We compared C-reactive protein, individual cytokines/chemokines and Cytokine Score to the outcomes: positivity for RF and for the HRP using logistic regression.RESULTSAdjusting for age, sex, ethnicity and ever smoking, the Cytokine Score and levels of IL-6 and IL-9 were associated with both RF and HRP. IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon (IFN)-γ were associated with HRP only. Associations between the Cytokine Score and RF and HRP positivity were replicated in an independent military personnel cohort.CONCLUSIONSIn first-degree relatives of patients with RA, RA-related autoimmunity is associated with inflammation, as evidenced by associations with multiple cytokines and chemokines. Objective We investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree relatives (FDRs) of RA probands, a population without RA but at increased risk for its future development. Methods We studied 44 autoantibody positive FDRs, of whom 29 were rheumatoid factor (RF) positive, 25 were positive for the high risk autoantibody profile (HRP), that is, positive for anti-cyclic citrullinated peptide and/or for at least two RF IgM, IgG or IgA isotypes, and nine FDRs who were positive for both; and 62 FDRs who were never autoantibody positive. Twenty-five cytokines/chemokines were measured using a bead-based assay in serum. As a comprehensive measure of inflammation, we calculated a Cytokine Score by summing all cytokine/chemokine levels, weighted by their regression coefficients for RA-autoantibody association. We compared C-reactive protein, individual cytokines/chemokines and Cytokine Score to the outcomes: positivity for RF and for the HRP using logistic regression. Results Adjusting for age, sex, ethnicity and ever smoking, the Cytokine Score and levels of IL-6 and IL-9 were associated with both RF and HRP. IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon (IFN)-γ were associated with HRP only. Associations between the Cytokine Score and RF and HRP positivity were replicated in an independent military personnel cohort. Conclusions In first-degree relatives of patients with RA, RA-related autoimmunity is associated with inflammation, as evidenced by associations with multiple cytokines and chemokines. Objective We investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree relatives (FDRs) of RA probands, a population without RA but at increased risk for its future development. Methods We studied 44 autoantibody positive FDRs, of whom 29 were rheumatoid factor (RF) positive, 25 were positive for the high risk autoantibody profile (HRP), that is, positive for anti-cyclic citrullinated peptide and/or for at least two RF IgM, IgG or IgA isotypes, and nine FDRs who were positive for both; and 62 FDRs who were never autoantibody positive. Twenty-five cytokines/chemokines were measured using a bead-based assay in serum. As a comprehensive measure of inflammation, we calculated a Cytokine Score by summing all cytokine/chemokine levels, weighted by their regression coefficients for RA-autoantibody association. We compared C-reactive protein, individual cytokines/chemokines and Cytokine Score to the outcomes: positivity for RF and for the HRP using logistic regression. Results Adjusting for age, sex, ethnicity and ever smoking, the Cytokine Score and levels of IL-6 and IL-9 were associated with both RF and HRP. IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon (IFN)-[GAMMA] were associated with HRP only. Associations between the Cytokine Score and RF and HRP positivity were replicated in an independent military personnel cohort. Conclusions In first-degree relatives of patients with RA, RA-related autoimmunity is associated with inflammation, as evidenced by associations with multiple cytokines and chemokines. |
| Author | Derber, Lezlie A Weisman, Michael H Zerbe, Gary O Gregersen, Peter K Norris, Jill M Holers, V Michael Mikuls, Ted R Sokolove, Jeremy Hughes-Austin, Jan M O'Dell, James R Deane, Kevin D Buckner, Jane H Lahey, Lauren J Robinson, William H Keating, Richard M Kolfenbach, Jason R |
| AuthorAffiliation | 4 VA Palo Alto Health Care System, Palo Alto, California and the Division of Rheumatology, Stanford University School of Medicine, Stanford, California, USA 3 Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, Colorado, USA 9 Robert S Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, New York, USA 7 Division of Rheumatology and Immunology, Omaha VA and University of Nebraska Medical Center, Omaha, Nebraska, USA 2 Division of Rheumatology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA 1 Department of Epidemiology, Colorado School of Public Health, Aurora, Colorado, USA 5 Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, California, USA 8 Section of Rheumatology, University of Chicago, Chicago, Illinois, USA 6 Translational Research Program, Benaroya Research Institute at Virginia Mason, Seattle, Washington, USA |
| AuthorAffiliation_xml | – name: 4 VA Palo Alto Health Care System, Palo Alto, California and the Division of Rheumatology, Stanford University School of Medicine, Stanford, California, USA – name: 2 Division of Rheumatology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA – name: 5 Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, California, USA – name: 3 Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, Colorado, USA – name: 1 Department of Epidemiology, Colorado School of Public Health, Aurora, Colorado, USA – name: 8 Section of Rheumatology, University of Chicago, Chicago, Illinois, USA – name: 6 Translational Research Program, Benaroya Research Institute at Virginia Mason, Seattle, Washington, USA – name: 7 Division of Rheumatology and Immunology, Omaha VA and University of Nebraska Medical Center, Omaha, Nebraska, USA – name: 9 Robert S Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, New York, USA |
| Author_xml | – sequence: 1 givenname: Jan M surname: Hughes-Austin fullname: Hughes-Austin, Jan M email: Jill.norris@ucdenver.edu organization: Department of Epidemiology, Colorado School of Public Health, Aurora, Colorado, USA – sequence: 2 givenname: Kevin D surname: Deane fullname: Deane, Kevin D email: Jill.norris@ucdenver.edu organization: Division of Rheumatology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA – sequence: 3 givenname: Lezlie A surname: Derber fullname: Derber, Lezlie A email: Jill.norris@ucdenver.edu organization: Division of Rheumatology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA – sequence: 4 givenname: Jason R surname: Kolfenbach fullname: Kolfenbach, Jason R email: Jill.norris@ucdenver.edu organization: Division of Rheumatology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA – sequence: 5 givenname: Gary O surname: Zerbe fullname: Zerbe, Gary O email: Jill.norris@ucdenver.edu organization: Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, Colorado, USA – sequence: 6 givenname: Jeremy surname: Sokolove fullname: Sokolove, Jeremy email: Jill.norris@ucdenver.edu organization: VA Palo Alto Health Care System, Palo Alto, California and the Division of Rheumatology, Stanford University School of Medicine, Stanford, California, USA – sequence: 7 givenname: Lauren J surname: Lahey fullname: Lahey, Lauren J email: Jill.norris@ucdenver.edu organization: VA Palo Alto Health Care System, Palo Alto, California and the Division of Rheumatology, Stanford University School of Medicine, Stanford, California, USA – sequence: 8 givenname: Michael H surname: Weisman fullname: Weisman, Michael H email: Jill.norris@ucdenver.edu organization: Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, California, USA – sequence: 9 givenname: Jane H surname: Buckner fullname: Buckner, Jane H email: Jill.norris@ucdenver.edu organization: Translational Research Program, Benaroya Research Institute at Virginia Mason, Seattle, Washington, USA – sequence: 10 givenname: Ted R surname: Mikuls fullname: Mikuls, Ted R email: Jill.norris@ucdenver.edu organization: Division of Rheumatology and Immunology, Omaha VA and University of Nebraska Medical Center, Omaha, Nebraska, USA – sequence: 11 givenname: James R surname: O'Dell fullname: O'Dell, James R email: Jill.norris@ucdenver.edu organization: Division of Rheumatology and Immunology, Omaha VA and University of Nebraska Medical Center, Omaha, Nebraska, USA – sequence: 12 givenname: Richard M surname: Keating fullname: Keating, Richard M email: Jill.norris@ucdenver.edu organization: Section of Rheumatology, University of Chicago, Chicago, Illinois, USA – sequence: 13 givenname: Peter K surname: Gregersen fullname: Gregersen, Peter K email: Jill.norris@ucdenver.edu organization: Robert S Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, New York, USA – sequence: 14 givenname: William H surname: Robinson fullname: Robinson, William H email: Jill.norris@ucdenver.edu organization: VA Palo Alto Health Care System, Palo Alto, California and the Division of Rheumatology, Stanford University School of Medicine, Stanford, California, USA – sequence: 15 givenname: V Michael surname: Holers fullname: Holers, V Michael email: Jill.norris@ucdenver.edu organization: Division of Rheumatology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA – sequence: 16 givenname: Jill M surname: Norris fullname: Norris, Jill M email: Jill.norris@ucdenver.edu organization: Department of Epidemiology, Colorado School of Public Health, Aurora, Colorado, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22915618$$D View this record in MEDLINE/PubMed |
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| DOI | 10.1136/annrheumdis-2012-201505 |
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| References | Khan, Krishnan, Ziman 2009; 76 Nielen, van Schaardenburg, Reesink 2006; 65 Vallbracht, Rieber, Oppermann 2004; 63 Jonsson, Valdimarsson 1992; 12 Arlestig, Mullazehi, Kokkonen 2012; 71 Nielen, van Schaardenburg, Reesink 2004; 50 Hueber, Tomooka, Zhao 2007; 66 Libby 2008; 121 Deighton, Wentzel, Cavanagh 1992; 51 Deane, O'Donnell, Hueber 2010; 62 Kokkonen, Soderstrom, Rocklov 2010; 62 Aho, Palosuo, Heliovaara 2000; 27 Todd, Knowlton, Amato 2011; 63 Jorgensen, Wiik, Pedersen 2008; 67 Szodoray, Alex, Chappell-Woodward 2007; 46 Aho, Palusuo, Kurki 1994; 23 DeForge, Loyet, Delarosa 2010; 362 Arnett, Edworthy, Bloch 1988; 31 Kolfenbach, Deane, Derber 2009; 61 Gerlag, Raza, van Baarsen 2012; 71 Berglin, Padyukov, Sundin 2004; 6 Snee 1977; 19 Rantapaa-Dahlqvist, de Jong, Berglin 2003; 48 Picard, Berk 1990; 44 Aletaha, Neogi, Silman 2010; 62 Jonsson, Steinsson, Jonsson 1998; 18 Rantapaa-Dahlqvist, de Jong, Hallmans 2002; 46 Wegner, Lundberg, Kinloch 2010; 233 Aho, Heliovaara, Maatela 1991; 18 del Puente, Knowler, Pettitt 1988; 31 2023052607101472000_72.6.901.15 2023052607101472000_72.6.901.16 2023052607101472000_72.6.901.17 2023052607101472000_72.6.901.18 Kokkonen (2023052607101472000_72.6.901.13) 2010; 62 2023052607101472000_72.6.901.19 Aho (2023052607101472000_72.6.901.5) 2000; 27 2023052607101472000_72.6.901.31 2023052607101472000_72.6.901.10 2023052607101472000_72.6.901.32 2023052607101472000_72.6.901.11 2023052607101472000_72.6.901.33 2023052607101472000_72.6.901.12 2023052607101472000_72.6.901.34 2023052607101472000_72.6.901.14 2023052607101472000_72.6.901.26 2023052607101472000_72.6.901.27 Aho (2023052607101472000_72.6.901.4) 1991; 18 2023052607101472000_72.6.901.28 2023052607101472000_72.6.901.29 2023052607101472000_72.6.901.1 2023052607101472000_72.6.901.3 2023052607101472000_72.6.901.20 2023052607101472000_72.6.901.2 2023052607101472000_72.6.901.21 2023052607101472000_72.6.901.22 2023052607101472000_72.6.901.23 2023052607101472000_72.6.901.24 Khan (2023052607101472000_72.6.901.30) 2009; 76 2023052607101472000_72.6.901.25 2023052607101472000_72.6.901.9 2023052607101472000_72.6.901.8 Rantapaa-Dahlqvist (2023052607101472000_72.6.901.7) 2002; 46 2023052607101472000_72.6.901.6 |
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rheumatoid arthritis publication-title: Arthritis Res Ther contributor: fullname: Sundin – volume: 12 start-page: 111 year: 1992 article-title: Clinical significance of rheumatoid factor isotypes in seropositive arthritis publication-title: Rheumatol Int contributor: fullname: Valdimarsson – volume: 51 start-page: 182 year: 1992 article-title: Contribution of inherited factors to rheumatoid arthritis publication-title: Ann Rheum Dis contributor: fullname: Cavanagh – volume: 76 start-page: 159 year: 2009 ident: 2023052607101472000_72.6.901.30 article-title: A comparison of multiplex suspension array large-panel kits for profiling cytokines and chemokines in rheumatoid arthritis patients publication-title: Cytometry Part B, Clin Cytom doi: 10.1002/cyto.b.20452 contributor: fullname: Khan – ident: 2023052607101472000_72.6.901.34 doi: 10.1002/art.27584 – volume: 62 start-page: 383 year: 2010 ident: 2023052607101472000_72.6.901.13 article-title: Up-regulation of cytokines and chemokines predates the onset of rheumatoid arthritis publication-title: Arthritis Rheum doi: 10.1002/art.27186 contributor: fullname: Kokkonen – ident: 2023052607101472000_72.6.901.8 doi: 10.1002/art.11223 – ident: 2023052607101472000_72.6.901.2 doi: 10.1111/j.0105-2896.2009.00850.x – ident: 2023052607101472000_72.6.901.14 doi: 10.1136/ard.2007.073825 – ident: 2023052607101472000_72.6.901.6 doi: 10.1002/art.1780311004 – ident: 2023052607101472000_72.6.901.3 doi: 10.1016/0049-0172(94)90088-4 – ident: 2023052607101472000_72.6.901.15 – volume: 46 start-page: S200 year: 2002 ident: 2023052607101472000_72.6.901.7 article-title: Antibodies against citrullinated peptides (CCP) predict the development of rheumatoid arthritis publication-title: Arthritis Rheum contributor: fullname: Rantapaa-Dahlqvist – ident: 2023052607101472000_72.6.901.9 doi: 10.1002/art.20018 – ident: 2023052607101472000_72.6.901.20 doi: 10.1007/s002960050069 – ident: 2023052607101472000_72.6.901.27 doi: 10.2307/1267881 – ident: 2023052607101472000_72.6.901.28 doi: 10.2307/2684155 – ident: 2023052607101472000_72.6.901.26 doi: 10.1002/art.30213 – volume: 27 start-page: 2743 year: 2000 ident: 2023052607101472000_72.6.901.5 article-title: Antifilaggrin antibodies within “normal” range predict rheumatoid arthritis in a linear fashion publication-title: J Rheumatol contributor: fullname: Aho – ident: 2023052607101472000_72.6.901.31 – ident: 2023052607101472000_72.6.901.29 – ident: 2023052607101472000_72.6.901.18 doi: 10.1002/art.1780310302 – ident: 2023052607101472000_72.6.901.1 doi: 10.1016/j.amjmed.2008.06.014 – ident: 2023052607101472000_72.6.901.17 doi: 10.1002/art.24833 – ident: 2023052607101472000_72.6.901.19 doi: 10.1136/ard.2003.019877 – ident: 2023052607101472000_72.6.901.12 doi: 10.1002/art.27638 – ident: 2023052607101472000_72.6.901.16 doi: 10.1136/ard.51.2.182 – volume: 18 start-page: 1282 year: 1991 ident: 2023052607101472000_72.6.901.4 article-title: Rheumatoid factors antedating clinical rheumatoid arthritis publication-title: J Rheumatol contributor: fullname: Aho – ident: 2023052607101472000_72.6.901.33 doi: 10.1136/annrheumdis-2011-200990 – ident: 2023052607101472000_72.6.901.11 doi: 10.1186/ar1187 – ident: 2023052607101472000_72.6.901.21 doi: 10.1007/BF00290265 – ident: 2023052607101472000_72.6.901.22 doi: 10.1136/ard.2006.054924 – ident: 2023052607101472000_72.6.901.10 doi: 10.1136/ard.2005.040659 – ident: 2023052607101472000_72.6.901.23 doi: 10.1016/j.jim.2010.09.004 – ident: 2023052607101472000_72.6.901.25 doi: 10.1093/rheumatology/kel306 – ident: 2023052607101472000_72.6.901.24 doi: 10.1002/art.30213 – ident: 2023052607101472000_72.6.901.32 doi: 10.1136/annrheumdis-2011-200668 |
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| Snippet | Objective We investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of... We investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of first-degree... OBJECTIVEWe investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of... ObjectiveWe investigated whether rheumatoid arthritis (RA)-related autoantibodies were associated with systemic inflammation in a prospective cohort of... |
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| SubjectTerms | Adult Aged Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - immunology Autoantibodies - immunology Autoimmunity - genetics Autoimmunity - immunology Biomarkers C-Reactive Protein - immunology Chemokines Chemokines - immunology Cohort Studies Cytokines Cytokines - immunology Female Genetic Predisposition to Disease Genotype & phenotype Granulocyte-Macrophage Colony-Stimulating Factor - immunology Health risk assessment Humans Inflammation Inflammation - immunology Interferon-gamma - immunology Interleukin-2 - immunology Interleukin-6 - immunology Interleukin-9 - immunology Logistic Models Male Middle Aged Peptides, Cyclic - immunology Phenotype Population Prospective Studies Rheumatoid arthritis Rheumatoid Factor - immunology Rheumatology Studies Tumor necrosis factor-TNF |
| Title | Multiple cytokines and chemokines are associated with rheumatoid arthritis-related autoimmunity in first-degree relatives without rheumatoid arthritis: Studies of the Aetiology of Rheumatoid Arthritis (SERA) |
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