期刊
CLINICAL & DEVELOPMENTAL IMMUNOLOGY
卷 -, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2012/780436
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资金
- K Ko-Arthritis Foundation Clinical to Research Transition Award: TB Niewold-NIH [R01 AR060861, K08 AI083790, P30 DK42086]
- NIAID Clinical Research Loan Repayment [AI071651]
- NIH CTSA Core Subsidy Grant
- CTSA Pilot Grants [UL1 RR024999]
- Lupus Research Institute Novel Research Grant
- Alliance for Lupus Research Target Identification in Lupus Grant
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multiple genetic risk factors, high levels of interferon alpha (IFN-alpha), and the production of autoantibodies against components of the cell nucleus. Interferon regulatory factor 5 (IRF5) is a transcription factor which induces the transcription of IFN-alpha and other cytokines, and genetic variants of IRF5 have been strongly linked to SLE pathogenesis. IRF5 functions downstream of Toll-like receptors and other microbial pattern-recognition receptors, and immune complexes made up of SLE-associated autoantibodies seem to function as a chronic endogenous stimulus to this pathway. In this paper, we discuss the physiologic role of IRF5 in immune defense and the ways in which IRF5 variants may contribute to the pathogenesis of human SLE. Recent data regarding the role of IRF5 in both serologic autoimmunity and the overproduction of IFN-alpha in human SLE are summarized. These data support a model in which SLE-risk variants of IRF5 participate in a feed-forward mechanism, predisposing to SLE-associated autoantibody formation, and subsequently facilitating IFN-alpha production downstream of Toll-like receptors stimulated by immune complexes composed of these autoantibodies.
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