期刊
IMMUNITY
卷 28, 期 1, 页码 18-28出版社
CELL PRESS
DOI: 10.1016/j.immuni.2007.12.004
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI036529] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [P01AR050256] Funding Source: NIH RePORTER
- NIAID NIH HHS [P01-AI36529] Funding Source: Medline
- NIAMS NIH HHS [P01-AR50256] Funding Source: Medline
B cells are essential for the development and pathogenesis of both systemic and organ-specific autoimmune diseases. Autoreactive B cells are typically thought of as sources of autoantibody, but their most important pathogenetic roles may be to present autoantigens to T cells and to secrete proinflammatory cytokines. A rate-limiting step in the genesis of autoimmunity then is the activation of autoreactive B cells. Here, mechanisms are discussed that normally prevent such activation and how they break down during disease. Integrating classic work with recent insights, emphasis is placed on efforts to pinpoint the precursor cells for autoantibody-secreting cells and the unique stimuli and pathways by which they are activated.
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