期刊
JOURNAL OF IMMUNOLOGY
卷 202, 期 8, 页码 2210-2219出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1801295
关键词
-
类别
资金
- National Institutes of Health (NIH)/National Institute of Allergy and Infectious Diseases [5U01Al101990]
- National Institutes of Health (NIH)/National Institute of Allergy and Infectious Diseases through NIH [U01AI01934, AI114780]
- NIH/National Institute of General Medical Sciences Grant [U54GM104938]
- NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases Grant [P30AR053483]
- Onassis Foundation under the Special Grant and Support Program for Scholars' Association Members [R ZO 006/2018-2019]
- Wellcome Trust [104079/Z/14/Z]
- BMA Foundation Vera Down grant (2013)
- BMA Foundation Margaret Temple grant (2017)
- National Institute for Health Research (NIHR) Oxford Biomedical Research Centre
- Nancy Taylor Foundation for Chronic Diseases
- NIH [P01 AI045757, U19 AI046130, U19 AI070352, P01 AI073748, P01 AI039671]
The aim of this study was to test whether autoantibodies against neurologic surface Ags are found in nonneurologic autoimmune diseases, indicating a broader loss of tolerance. Patient and matched healthy donor (HD) sera were derived from four large cohorts: 1) rheumatoid arthritis (RA) (n = 194, HD n = 64), 2) type 1 diabetes (T1D) (n = 200, HD n = 200), 3) systemic lupus erythematosus (SLE) (n = 200, HD n = 67; neuro-SLE n = 49, HD n = 33), and 4) a control cohort of neurologic autoimmunity (relapsing-remitting multiple sclerosis [MS] n = 110, HD n = 110; primary progressive MS n = 9; secondary progressive MS n = 10; neuromyelitis optica spectrum disorders n = 15; and other neurologic disorders n = 26). Screening of 1287 unique serum samples against four neurologic surface Ags (myelin oligodendrocyte glycoprotein, aquaporin 4, acetylcholine receptor, and muscle-specific kinase) was performed with live cell-based immunofluorescence assays using flow cytometry. Positive samples identified in the screening were further validated using autoantibody titer quantification by serial dilutions or radioimmunoassay. Autoantibodies against neurologic surface Ags were not observed in RA and T1D patients, whereas SLE patients harbored such autoantibodies in rare cases (2/200, 1%). Within the CNS autoimmunity control cohort, autoantibodies against aquaporin 4 and high-titer Abs against myelin oligodendrocyte glycoprotein were, as expected, specific for neuromyelitis optica spectrum disorders. We conclude that neurologic autoantibodies do not cross disease barriers in RA and T1D. The finding of mildly increased neurologic autoantibodies in SLE may be consistent with a broader loss of B cell tolerance in this form of systemic autoimmunity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据