Organ-specific disease provoked by systemic autoimmunity
Organ-specific disease provoked by systemic autoimmunity
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DOI：
10.1016/s0092-8674(00)81989-3
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发表时间：
1996-11-29
期刊：
影响因子：
64.5
通讯作者：
Mathis, D
中科院分区：
文献类型：
--
作者：
Kouskoff, V;Korganow, AS;Mathis, D
Rheumatoid arthritis (RA) is a chronic joint disease characterized by leukocyte invasion and synoviocyte activation followed by cartilage and bone destruction. Its etiology and pathogenesis are poorly understood. We describe a spontaneous mouse model of this syndrome, generated fortuitously by crossing a T cell receptor (TCR) transgenic line with the NOD strain. All offspring develop a joint disease highly reminiscent of RA in man. The trigger for the murine disorder is chance recognition of a NOD-derived major histocompatibility complex (MHC) class II molecule by the transgenic TCR; progression to arthritis involves CD4+ T, B, and probably myeloid cells. Thus, a joint-specific disease need not arise from response to a joint-specific antigen but can be precipitated by a breakdown in general mechanisms of self-tolerance resulting in systemic self-reactivity. We suggest that human RA develops by an analogous mechanism.
