Published in:
01-02-2000 | Commentary
A revival of the B cell paradigm for rheumatoid arthritis pathogenesis?
Authors:
Christophe Benoist, Diane Mathis
Published in:
Arthritis Research & Therapy
|
Issue 2/2000
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Abstract
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.