期刊
CURRENT OPINION IN IMMUNOLOGY
卷 33, 期 -, 页码 70-77出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2015.01.018
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资金
- NHLBI
- NICHD
- NIDDK
- NIAID of the National Institutes of Health [R0IHL075453, R01AI084457, R01AI071163, DP3DK097672, K08AI112993]
- Benaroya Family Gift Fund
- Cancer Research Institute Pre-doctoral Training Grant
- ACR REF Rheumatology Scientist Development Award
- Arnold Lee Smith Endowed Professorship for Research Faculty Development
A significant proportion of autoimmune-associated genetic variants are expressed in B cells, suggesting that B cells may play multiple roles in autoimmune pathogenesis. In this review, we highlight recent studies demonstrating that even modest alterations in B cell signaling are sufficient to promote autoimmunity. First, we describe several examples of genetic variations promoting B cell-intrinsic initiation of autoimmune germinal centers and autoantibody production. We highlight how dual antigen receptor/toll-like receptor signals greatly facilitate this process and how activated, self-reactive B cells may function as antigen presenting cells, leading to loss of T cell tolerance. Further, we propose that B cell-derived cytokines may initiate and/or sustain autoimmune germinal centers, likely also contributing, in parallel, to programing of self-reactive T cells.
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