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Immunity. 1999 Apr;10(4):451-61.

From systemic T cell self-reactivity to organ-specific autoimmune disease via immunoglobulins.

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Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, C. U. de Strasbourg, France.


Rheumatoid arthritis is a common and debilitating autoimmune disease whose cause and mechanism remain a mystery. We recently described a T cell receptor transgenic mouse model that spontaneously develops a disease with most of the clinical, histological, and immunological features of rheumatoid arthritis in humans. Disease development in K/BxN mice is initiated by systemic T cell self-reactivity; it requires T cells, as expected, but B cells are also needed, more surprisingly. Here, we have identified the role of B cells as the secretion of arthritogenic immunoglobulins. We suggest that a similar scenario may unfold in some other arthritis models and in human patients, beginning with pervasive T cell autoreactivity and ending in immunoglobulin-provoked joint destruction.

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