期刊
TRENDS IN MOLECULAR MEDICINE
卷 21, 期 4, 页码 233-244出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2015.02.006
关键词
microbiome; commensal; bystander activation; epitope spread crossreactivity; molecular mimicry
资金
- National Institutes of Health (NIH) [K08 AI095318]
- Yale Rheumatic Diseases Research Core [NIH P30 AR053495]
- Women's Health Research at Yale
- O'Brien Center at Yale [NIH P30DK079310]
- Arthritis National Research Foundation
- Yale Interdisciplinary Immunology Training Program [NIH T32AI07019]
The microbiota is considered to be an important factor influencing the pathogenesis of autoimmunity at both barrier sites and internal organs. Impinging on innate and adaptive immunity, commensals exert protective or detrimental effects on various autoimmune animal models. Human microbiome studies of autoimmunity remain largely descriptive, but suggest a role for dysbiosis in autoimmune disease. Humanized gnotobiotic approaches have advanced our understanding of immune-commensal interactions, but little is known about the mechanisms in autoimmunity. We propose that, similarly to infectious agents, the microbiota mediates autoimmunity via bystander activation, epitope spread, and, particularly under homeostatic conditions, via crossreactivity. This review presents an overview of the current literature concluding with outstanding questions in this field.
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