Journal
IMMUNITY
Volume 28, Issue 1, Pages 18-28Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2007.12.004
Keywords
-
Categories
Funding
- 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
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available