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B cells flying solo
Author(s) -
Groom Joanna,
Mackay Fabienne
Publication year - 2008
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/sj.icb.7100142
Subject(s) - computer science
Systemic autoimmunity such as systemic lupus erythematosus (SLE) is associated with the loss of B‐cell tolerance, B‐cell dysregulation and autoantibody production. While some autoantibodies may contribute to the pathology seen with SLE, numerous studies have shown that dysregulation of T‐cell function is another critical aspect driving disease. The positive results obtained in clinical trials using T‐cell‐ or B‐cell‐specific treatments have suggested that cooperation between T and B cells probably underlies disease progression in many patients. A similar cooperative mechanism seemed to explain SLE developing in mice overexpressing the B‐cell‐activating factor from the tumor necrosis factor family (BAFF). However, surprisingly, T‐cell‐deficient BAFF transgenic (Tg) mice develop SLE similar to T‐cell‐sufficient BAFF Tg mice, and the disease was linked to innate activation of B cells and production of proinflammatory autoantibody isotypes. In conclusion, dysregulated innate activation of B cells alone can drive disease independently of T cells, and as such this aspect represents a new pathogenic mechanism in autoimmunity.