Anti-Ro52 positivity is associated with progressive interstitial lung disease in systemic sclerosis—an exploratory study
Background Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage...
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| Published in | Arthritis research & therapy Vol. 25; no. 1; pp. 1 - 13 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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London
BioMed Central Ltd
04.09.2023
BioMed Central BMC |
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| Abstract | Background Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD. Methods Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry. Results Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc. Conclusions This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. Keywords: Systemic sclerosis, Interstitial lung disease, Ro52, Autoantibody, Biomarker |
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| AbstractList | Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD.BACKGROUNDInterstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD.Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry.METHODSFifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry.Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc.RESULTSAmong SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc.This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD.CONCLUSIONSThis study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. BackgroundInterstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD.MethodsFifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry.ResultsAmong SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc.ConclusionsThis study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. BACKGROUND: Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD.METHODS: Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry.RESULTS: Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc.CONCLUSIONS: This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. Abstract Background Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD. Methods Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry. Results Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc. Conclusions This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. Background: Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD. Methods: Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry. Results: Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc. Conclusions: This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. Background Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD. Methods Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry. Results Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc. Conclusions This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. Keywords: Systemic sclerosis, Interstitial lung disease, Ro52, Autoantibody, Biomarker Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD. Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of the Ro52 antigen using immunohistochemistry. Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc. This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. BACKGROUND: Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify SSc-ILD patients at risk for progressive pulmonary fibrosis. This study investigates autoantibodies measured in bronchoalveolar lavage (BAL) fluid and in serum in reference to the clinical disease course of SSc-ILD. METHODS: Fifteen patients with new onset SSc-ILD underwent bronchoscopy. Autoantibody levels were analyzed using addressable laser bead immunoassay from BAL fluid and the serum. In a separate longitudinal cohort of 43 patients with early SSc-ILD, autoantibodies in serum were measured at baseline and pulmonary function tests were performed at least 2 times over the course of at least 2 or more years. Linear mixed effect models were created to investigate the relationship between specific autoantibodies and progression of SSc-ILD. Finally, lung tissue from healthy controls and from subjects with SSc was analyzed for the presence of theRo52 antigen using immunohistochemistry. RESULTS: Among SSc-ILD patients who were positive for anti-Ro52 (N = 5), 3 (60%) had enrichment of anti-Ro52 in BAL fluid at a ratio exceeding 50x. In the longitudinal cohort, 10/43 patients (23%) were anti-Ro52 positive and 16/43 (37%) were anti-scl-70 positive. Presence of anti-Scl-70 was associated with a lower vital capacity (VC) at baseline (-12.6% predicted VC [%pVC]; 95%CI: -25.0, -0.29; p = 0.045), but was not significantly associated with loss of lung function over time (-1.07%pVC/year; 95%CI: -2.86, 0.71; p = 0.230). The presence of anti-Ro52 was significantly associated with the loss of lung function over time (-2.41%pVC/year; 95% CI: -4.28, -0.54; p = 0.013). Rate of loss of lung function increased linearly with increasing anti-Ro52 antibody levels (-0.03%pVC per arbitrary units/mL and year; 95%CI: -0.05, -0.02; p < 0.001). Immunohistochemical staining localized the Ro52 antigen to alveolar M2 macrophages in peripheral lung tissue both in subjects with and without SSc. CONCLUSIONS: This study suggests that antibodies targeting Ro52 are enriched in the lungs of patients with new-onset SSc-ILD, linking Ro52 autoimmunity to the pulmonary pathology of SSc. Clinical and immunohistochemical data corroborates these findings and suggest that anti-Ro52 may serve as a potential biomarker of progressive SSc-ILD. |
| ArticleNumber | 162 |
| Audience | Academic |
| Author | Hamberg, Viggo Hesselstrand, Roger Dellgren, Göran Wildt, Marie Volkmann, Elizabeth R. Löfdahl, Anna Wuttge, Dirk M. Westergren-Thorsson, Gunilla Rönnelid, Johan Sohrabian, Azita Andréasson, Kristofer |
| Author_xml | – sequence: 1 givenname: Viggo surname: Hamberg fullname: Hamberg, Viggo – sequence: 2 givenname: Azita surname: Sohrabian fullname: Sohrabian, Azita – sequence: 3 givenname: Elizabeth R. surname: Volkmann fullname: Volkmann, Elizabeth R. – sequence: 4 givenname: Marie surname: Wildt fullname: Wildt, Marie – sequence: 5 givenname: Anna surname: Löfdahl fullname: Löfdahl, Anna – sequence: 6 givenname: Dirk M. surname: Wuttge fullname: Wuttge, Dirk M. – sequence: 7 givenname: Roger surname: Hesselstrand fullname: Hesselstrand, Roger – sequence: 8 givenname: Göran surname: Dellgren fullname: Dellgren, Göran – sequence: 9 givenname: Gunilla surname: Westergren-Thorsson fullname: Westergren-Thorsson, Gunilla – sequence: 10 givenname: Johan surname: Rönnelid fullname: Rönnelid, Johan – sequence: 11 givenname: Kristofer surname: Andréasson fullname: Andréasson, Kristofer |
| BackLink | https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-514917$$DView record from Swedish Publication Index https://gup.ub.gu.se/publication/335504$$DView record from Swedish Publication Index https://lup.lub.lu.se/record/52cc3349-20f0-4618-b7ea-ce3c670802b8$$DView record from Swedish Publication Index oai:portal.research.lu.se:publications/52cc3349-20f0-4618-b7ea-ce3c670802b8$$DView record from Swedish Publication Index |
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| CitedBy_id | crossref_primary_10_1016_j_autrev_2024_103600 crossref_primary_10_3389_fmed_2024_1340310 crossref_primary_10_1093_cei_uxae098 crossref_primary_10_1093_rheumatology_keae083 crossref_primary_10_1002_art_43120 crossref_primary_10_1097_BOR_0000000000001035 crossref_primary_10_1097_MS9_0000000000002032 crossref_primary_10_3389_fimmu_2024_1410661 crossref_primary_10_3389_fimmu_2024_1435525 crossref_primary_10_1016_j_autrev_2024_103536 |
| Cites_doi | 10.1016/j.autrev.2011.03.004 10.1056/NEJMoa055120 10.1183/09031936.00135205 10.1016/S2213-2600(16)30152-7 10.1002/art.41933 10.1136/ard.2006.066068 10.1183/13993003.02026-2019 10.1186/s12931-019-1231-7 10.1186/1465-9921-7-11 10.1002/art.41668 10.1111/cei.13211 10.1177/2397198319889549 10.1093/rheumatology/keaa550 10.1007/s00296-009-0884-9 10.1074/jbc.M111.241786 10.5301/jsrd.5000249 10.1093/rheumatology/kev016 10.1002/art.1780230510 10.1016/j.jaut.2012.05.002 10.1007/978-1-4614-4292-9_16 10.1002/art.38201 10.1007/s12016-021-08911-z 10.2147/CLEP.S191418 10.1016/j.jaut.2012.01.014 10.1016/j.cca.2017.10.002 10.1080/14397595.2017.1374235 10.18637/jss.v067.i01 10.1136/annrheumdis-2015-207259.13 10.1002/art.38098 10.1007/s00281-015-0507-3 10.1371/journal.pone.0103609 10.1016/j.semarthrit.2016.02.005 10.1016/j.pathol.2016.04.004 10.1016/j.rmed.2013.03.015 10.1093/rheumatology/40.10.1135 10.1016/j.autrev.2009.02.010 10.1136/annrheumdis-2020-217455 10.1136/annrheumdis-2017-211448 10.1093/rheumatology/kez230 10.1136/annrheumdis-2018-214436 10.1080/08916930600623791 10.3389/fimmu.2019.00444 10.1056/NEJMoa1903076 10.1016/S0140-6736(22)01692-0 10.1111/imm.12910 10.1164/rccm.202103-0714OC 10.1016/j.ejim.2021.04.020 10.1002/art.1780370903 10.1136/ard.2006.062901 10.1016/j.semarthrit.2011.09.008 10.1186/s13075-019-2056-y 10.1136/ard.61.10.929 10.1056/NEJMc1910735 10.1093/rheumatology/kev300 10.1183/16000617.0340-2020 10.1183/09031936.00080312 10.1186/ar3125 10.1186/ar3763 10.3390/jcm12103428 |
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| CorporateAuthor | Thoraxkirurgi Lung Biology WCMM-Wallenberg Centre for Molecular Medicine Reumatologi och molekylär skelettbiologi WCMM- Wallenberg center för molekylär medicinsk forskning Department of Clinical Sciences, Lund Strategiska forskningsområden (SFO) Hjärt-lungsjukdom - information, stöd och bemötande Section III Medicinska fakulteten Forskargruppen för systemisk skleros, Lund Lungbiologi Rheumatology Institutionen för kliniska vetenskaper, Lund Sektion II Lunds universitet Institutionen för experimentell medicinsk vetenskap Section II Profile areas and other strong research environments Thoracic Surgery Lund University Sektion III Lund University Bioimaging Center Department of Experimental Medical Science Cardiopulmonary disease - information, support and reception Faculty of Medicine Strategic research areas (SRA) eSSENCE: The e-Science Collaboration Lund Systemic Sclerosis Research Group Profilområden och andra starka forskningsmiljöer |
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| References | 3141_CR37 K Andreasson (3141_CR13) 2019; 381 DP Tashkin (3141_CR6) 2016; 4 3141_CR32 AM Hoffmann-Vold (3141_CR36) 2021; 80 A Robbins (3141_CR47) 2019; 10 P Ghillani (3141_CR53) 2011; 10 VD Steen (3141_CR1) 2007; 66 RP Goswami (3141_CR10) 2021; 60 3141_CR38 J Varga (3141_CR16) 2017; 2 F van den Hoogen (3141_CR26) 2013; 65 AT Masi (3141_CR25) 1980; 23 O Distler (3141_CR9) 2019; 380 A Váncsa (3141_CR41) 2009; 29 M Hudson (3141_CR22) 2012; 14 M Infantino (3141_CR64) 2017; 475 A Bergamasco (3141_CR3) 2019; 11 A Scheja (3141_CR27) 2007; 29 I Peene (3141_CR44) 2002; 61 O Bonhomme (3141_CR63) 2019; 58 S Brauner (3141_CR61) 2018; 194 3141_CR65 EKL Chan (3141_CR49) 2022; 63 D Bates (3141_CR39) 2015; 67 A Espinosa (3141_CR59) 2011; 286 P Decker (3141_CR21) 2021; 91 V Oke (3141_CR23) 2012; 39 FW Miller (3141_CR56) 2012; 39 3141_CR62 A Sclafani (3141_CR54) 2019; 20 PJ Clements (3141_CR30) 1993; 20 M Elhai (3141_CR4) 2017; 76 G Reynisdottir (3141_CR24) 2014; 66 3141_CR15 3141_CR57 S Sato (3141_CR52) 2001; 40 3141_CR5 R Gunnarsson (3141_CR40) 2016; 55 I Marie (3141_CR50) 2012; 41 J Damoiseaux (3141_CR35) 2019; 78 SC Funes (3141_CR58) 2018; 154 ER Volkmann (3141_CR17) 2020; 5 EC LeRoy (3141_CR31) 1988; 15 PD Burbelo (3141_CR46) 2010; 2 A Man (3141_CR7) 2015; 54 D Khanna (3141_CR11) 2022; 205 D Chandratilleke (3141_CR48) 2016; 48 R La Corte (3141_CR43) 2006; 39 PH Quanjer (3141_CR33) 2012; 40 UA Walker (3141_CR18) 2007; 66 3141_CR42 DP Tashkin (3141_CR8) 2006; 354 D Roofeh (3141_CR12) 2021; 73 VD Steen (3141_CR14) 1994; 37 S Assassi (3141_CR19) 2010; 12 C Frantz (3141_CR2) 2016; 46 M Wodkowski (3141_CR20) 2015; 33 M Miyasato-Isoda (3141_CR51) 2018; 28 K Larsen (3141_CR28) 2006; 7 I Marie (3141_CR55) 2015; 37 A Sohrabian (3141_CR34) 2019; 21 R Hesselstrand (3141_CR29) 2013; 107 J Schulte-Pelkum (3141_CR45) 2009; 8 E Lazzari (3141_CR60) 2014; 9 |
| References_xml | – volume: 15 start-page: 202 issue: 2 year: 1988 ident: 3141_CR31 publication-title: J Rheumatol – volume: 10 start-page: 509 issue: 9 year: 2011 ident: 3141_CR53 publication-title: Autoimmun Rev doi: 10.1016/j.autrev.2011.03.004 – volume: 354 start-page: 2655 issue: 25 year: 2006 ident: 3141_CR8 publication-title: N Engl J Med doi: 10.1056/NEJMoa055120 – volume: 29 start-page: 446 issue: 3 year: 2007 ident: 3141_CR27 publication-title: Eur Respir J doi: 10.1183/09031936.00135205 – volume: 4 start-page: 708 issue: 9 year: 2016 ident: 3141_CR6 publication-title: Lancet Respir Med doi: 10.1016/S2213-2600(16)30152-7 – ident: 3141_CR65 doi: 10.1002/art.41933 – volume: 66 start-page: 940 issue: 7 year: 2007 ident: 3141_CR1 publication-title: Ann Rheum Dis doi: 10.1136/ard.2006.066068 – ident: 3141_CR37 doi: 10.1183/13993003.02026-2019 – volume: 20 start-page: 256 issue: 1 year: 2019 ident: 3141_CR54 publication-title: Respir Res doi: 10.1186/s12931-019-1231-7 – volume: 7 start-page: 11 issue: 1 year: 2006 ident: 3141_CR28 publication-title: Respir Res doi: 10.1186/1465-9921-7-11 – volume: 73 start-page: 1301 issue: 7 year: 2021 ident: 3141_CR12 publication-title: Arthritis Rheumatol doi: 10.1002/art.41668 – volume: 194 start-page: 315 issue: 3 year: 2018 ident: 3141_CR61 publication-title: Clin Exp Immunol doi: 10.1111/cei.13211 – volume: 5 start-page: 31 issue: 2 Suppl year: 2020 ident: 3141_CR17 publication-title: J Scleroderma Relat Disord doi: 10.1177/2397198319889549 – volume: 60 start-page: 557 issue: 2 year: 2021 ident: 3141_CR10 publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/keaa550 – volume: 29 start-page: 989 issue: 9 year: 2009 ident: 3141_CR41 publication-title: Rheumatol Int doi: 10.1007/s00296-009-0884-9 – volume: 286 start-page: 36478 issue: 42 year: 2011 ident: 3141_CR59 publication-title: J Biol Chem doi: 10.1074/jbc.M111.241786 – volume: 2 start-page: 137 issue: 3 year: 2017 ident: 3141_CR16 publication-title: J Scleroderma and Relat Disord doi: 10.5301/jsrd.5000249 – volume: 54 start-page: 1464 issue: 8 year: 2015 ident: 3141_CR7 publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/kev016 – volume: 23 start-page: 581 issue: 5 year: 1980 ident: 3141_CR25 publication-title: Arthritis Rheum doi: 10.1002/art.1780230510 – volume: 39 start-page: 259 issue: 4 year: 2012 ident: 3141_CR56 publication-title: J Autoimmun doi: 10.1016/j.jaut.2012.05.002 – volume: 20 start-page: 1892 issue: 11 year: 1993 ident: 3141_CR30 publication-title: J Rheumatol – ident: 3141_CR32 doi: 10.1007/978-1-4614-4292-9_16 – volume: 66 start-page: 31 issue: 1 year: 2014 ident: 3141_CR24 publication-title: Arthritis Rheumatol doi: 10.1002/art.38201 – ident: 3141_CR38 – volume: 63 start-page: 178 issue: 2 year: 2022 ident: 3141_CR49 publication-title: Clin Rev Allergy Immunol doi: 10.1007/s12016-021-08911-z – volume: 11 start-page: 257 year: 2019 ident: 3141_CR3 publication-title: Clin Epidemiol doi: 10.2147/CLEP.S191418 – volume: 39 start-page: 77 issue: 1–2 year: 2012 ident: 3141_CR23 publication-title: J Autoimmun doi: 10.1016/j.jaut.2012.01.014 – volume: 475 start-page: 15 year: 2017 ident: 3141_CR64 publication-title: Clin Chim Acta doi: 10.1016/j.cca.2017.10.002 – volume: 33 start-page: S131 issue: 4 Suppl 91 year: 2015 ident: 3141_CR20 publication-title: Clin Exp Rheumatol – volume: 28 start-page: 690 issue: 4 year: 2018 ident: 3141_CR51 publication-title: Mod Rheumatol doi: 10.1080/14397595.2017.1374235 – volume: 67 start-page: 1 issue: 1 year: 2015 ident: 3141_CR39 publication-title: J Stat Softw doi: 10.18637/jss.v067.i01 – ident: 3141_CR57 doi: 10.1136/annrheumdis-2015-207259.13 – volume: 65 start-page: 2737 issue: 11 year: 2013 ident: 3141_CR26 publication-title: Arthritis Rheum doi: 10.1002/art.38098 – volume: 37 start-page: 463 issue: 5 year: 2015 ident: 3141_CR55 publication-title: Semin Immunopathol doi: 10.1007/s00281-015-0507-3 – volume: 9 issue: 8 year: 2014 ident: 3141_CR60 publication-title: PLoS ONE doi: 10.1371/journal.pone.0103609 – volume: 46 start-page: 115 issue: 1 year: 2016 ident: 3141_CR2 publication-title: Semin Arthritis Rheum doi: 10.1016/j.semarthrit.2016.02.005 – volume: 48 start-page: 491 issue: 5 year: 2016 ident: 3141_CR48 publication-title: Pathology doi: 10.1016/j.pathol.2016.04.004 – volume: 107 start-page: 1079 issue: 7 year: 2013 ident: 3141_CR29 publication-title: Respir Med doi: 10.1016/j.rmed.2013.03.015 – volume: 40 start-page: 1135 issue: 10 year: 2001 ident: 3141_CR52 publication-title: Rheumatology doi: 10.1093/rheumatology/40.10.1135 – volume: 8 start-page: 632 issue: 7 year: 2009 ident: 3141_CR45 publication-title: Autoimmun Rev doi: 10.1016/j.autrev.2009.02.010 – volume: 80 start-page: 219 issue: 2 year: 2021 ident: 3141_CR36 publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2020-217455 – volume: 76 start-page: 1897 issue: 11 year: 2017 ident: 3141_CR4 publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2017-211448 – volume: 58 start-page: 1534 issue: 9 year: 2019 ident: 3141_CR63 publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/kez230 – volume: 78 start-page: 879 issue: 7 year: 2019 ident: 3141_CR35 publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2018-214436 – volume: 39 start-page: 249 issue: 3 year: 2006 ident: 3141_CR43 publication-title: Autoimmunity doi: 10.1080/08916930600623791 – volume: 10 start-page: 444 year: 2019 ident: 3141_CR47 publication-title: Front Immunol doi: 10.3389/fimmu.2019.00444 – volume: 380 start-page: 2518 issue: 26 year: 2019 ident: 3141_CR9 publication-title: N Engl J Med doi: 10.1056/NEJMoa1903076 – ident: 3141_CR5 doi: 10.1016/S0140-6736(22)01692-0 – volume: 154 start-page: 186 issue: 2 year: 2018 ident: 3141_CR58 publication-title: Immunology doi: 10.1111/imm.12910 – ident: 3141_CR15 – volume: 205 start-page: 674 issue: 6 year: 2022 ident: 3141_CR11 publication-title: Am J Respir Crit Care Med doi: 10.1164/rccm.202103-0714OC – volume: 91 start-page: 45 year: 2021 ident: 3141_CR21 publication-title: Eur J Intern Med doi: 10.1016/j.ejim.2021.04.020 – volume: 37 start-page: 1283 issue: 9 year: 1994 ident: 3141_CR14 publication-title: Arthritis Rheum doi: 10.1002/art.1780370903 – volume: 66 start-page: 754 issue: 6 year: 2007 ident: 3141_CR18 publication-title: Ann Rheum Dis doi: 10.1136/ard.2006.062901 – volume: 41 start-page: 890 issue: 6 year: 2012 ident: 3141_CR50 publication-title: Semin Arthritis Rheum doi: 10.1016/j.semarthrit.2011.09.008 – volume: 21 start-page: 259 issue: 1 year: 2019 ident: 3141_CR34 publication-title: Arthritis Res Ther doi: 10.1186/s13075-019-2056-y – volume: 61 start-page: 929 issue: 10 year: 2002 ident: 3141_CR44 publication-title: Ann Rheum Dis doi: 10.1136/ard.61.10.929 – volume: 2 start-page: 145 issue: 2 year: 2010 ident: 3141_CR46 publication-title: Am J Transl Res – volume: 381 start-page: 1595 issue: 16 year: 2019 ident: 3141_CR13 publication-title: N Engl J Med doi: 10.1056/NEJMc1910735 – volume: 55 start-page: 103 issue: 1 year: 2016 ident: 3141_CR40 publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/kev300 – ident: 3141_CR62 doi: 10.1183/16000617.0340-2020 – volume: 40 start-page: 1324 issue: 6 year: 2012 ident: 3141_CR33 publication-title: Eur Respir J doi: 10.1183/09031936.00080312 – volume: 12 start-page: R166 issue: 5 year: 2010 ident: 3141_CR19 publication-title: Arthritis Res Ther doi: 10.1186/ar3125 – volume: 14 start-page: R50 issue: 2 year: 2012 ident: 3141_CR22 publication-title: Arthritis Res Ther doi: 10.1186/ar3763 – ident: 3141_CR42 doi: 10.3390/jcm12103428 |
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| Snippet | Background Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to... Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to identify... BackgroundInterstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to... Background: Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to... BACKGROUND: Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are needed to... Abstract Background Interstitial lung disease (ILD) is the most common cause of death in patients with systemic sclerosis (SSc). Prognostic biomarkers are... |
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| Title | Anti-Ro52 positivity is associated with progressive interstitial lung disease in systemic sclerosis—an exploratory study |
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