| Autor: |
de Winter JJ; Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands., Blijdorp IC; Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands.; Laboratory of Experimental Immunology, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands., de Jong HM; Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands., Sauter J; DKMS German Bone Marrow Donor Center, Tübingen, Germany., Schmidt AH; DKMS German Bone Marrow Donor Center, Tübingen, Germany., van Gaalen FA; Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands., van der Heijde D; Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands., Poddubnyy D; Department of Rheumatology, Charité Universitätsmedizin Berlin, Berlin, Germany., Yeremenko NG; Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands.; Laboratory of Experimental Immunology, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands., van de Sande MG; Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands., Baeten DL; Department of Clinical Immunology and Rheumatology, Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands. d.l.baeten@amc.uva.nl. |
| Abstrakt: |
We aimed to assess the mRNA expression of MHC class 1-related molecules in ankylosing spondylitis (AS) patients vs healthy controls (HCs) and, subsequently, if the absence of HLA-C*07 is associated with genetic susceptibility to axial spondyloarthritis (axSpA). HLA-C*07 was assessed in (a) an exploratory cohort of 24 AS patients vs 40 HCs, (b) a confirmatory cohort of 113 AS patients and 83 non-radiographic axSpA patients from the GErman SPondyloarthritis Inception Cohort (GESPIC) vs 134,528 German potential stem cell donors, and (c) an early back pain cohort with 94 early axSpA patients vs 216 chronic back pain (CBP) patients from the SPondyloArthritis Caught Early (SPACE) cohort. In the exploratory cohort, 79% of the AS patients were HLA-C*07 negative compared to 35% of the HCs (p < 0.001). This difference was confirmed in GESPIC with 73% of AS patients being HLA-C*07 negative compared to 50% of the controls (p < 0.0001); 59% of the nr-axSpA patients were HLA-C*07 negative. In the SPACE cohort, 70% of the axSpA patients were HLA-C*07 negative compared to 44% of CBP patients (p < 0.0001); the association between HLA-C*07 negativity and a diagnosis of axSpA was independent from HLA-B*27. In conclusion, the absence of HLA-C*07 is associated with genetic susceptibility to axSpA. |
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