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A revival of the B cell paradigm for rheumatoid arthritis pathogenesis?

Published by National Institutes of Health | U.S. Department of Health & Human Services | Catalog Last Checked: July 31, 2026 at 09:43 PM | Dataset Last Updated: September 06, 2025
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.

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