A revival of the B cell paradigm for rheumatoid arthritis pathogenesis?
Dominant paradigms for the understanding of rheumatoid arthritis (RA) pathogenesis have changed over the years. A predominant role of B lymphocytes, and perhaps of the rheumatoid factor they produced, was initially invoked. In more recent years, recognition of antigens in the joint by T cells sparking an inflammatory cascade has been a more favored interpretation. Here, we re-examine some of the arguments that underpin this proposed role of joint T cells, in light of recent results from transgenic mice in which a self-reactive T-cell receptor provokes disease, but from outside the joint and indirectly via B lymphocytes and immunoglobulins.
Benoist
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Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 02215, USA. cbdm@joslin.harvard.edu
Mathis
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D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000503:physiopathology*; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology*; D004195:Disease Models, Animal; D006801:Humans; D007136:Immunoglobulins / Q000276:immunology; D008285:Major Histocompatibility Complex / Q000276:immunology; D051379:Mice; D008822:Mice, Transgenic; D011948:Receptors, Antigen, T-Cell / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*
D007136:Immunoglobulins; D011948:Receptors, Antigen, T-Cell