期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 122, 期 4, 页码 1180-1188出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI58649
关键词
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资金
- NIH [U19 AI07035, P01 AI07374, P01 AI04575, RC2 NS07034, CA 1061-A-18, U19 AI08999, R01 AI09156, P01 AI03967, TG T32GM07205]
- Nancy Taylor Foundation for Chronic Diseases
Multiple sclerosis (MS) is a multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual. While the formation and persistence of meningeal lymphoid follicles suggest persistence of antigens to drive the continuing inflammatory and humoral response, the identity of an antigen or infectious agent leading to the oligoclonal expansion of B and T cells is unknown. In this review we examine new paradigms for understanding the immunopathology of MS, present recent data defining the common genetic variants underlying disease susceptibility, and explore how improved understanding of immune pathway disruption can inform MS prognosis and treatment decisions.
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