Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3391843 | Seminars in Immunology | 2006 | 8 Pages |
Abstract
A point mutation of the gene encoding ZAP-70, a key signal transduction molecule in T cells, results in spontaneous development of T cell-mediated autoimmune arthritis in mice homozygous for the mutation. The genetic anomaly alters differentiation and selection of T cells in the thymus, leading to thymic production of arthritogenic autoimmune T cells. The arthritogenic T cells persist in the periphery and elicit arthritis when activated by microbial agents that stimulate innate immunity. This model is instrumental in understanding how genetic variations in T cell signal transduction, together with environmental influences, contribute to the development of autoimmune disease.
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Immunology
Authors
Shimon Sakaguchi, Noriko Sakaguchi, Hiroyuki Yoshitomi, Hiroshi Hata, Takeshi Takahashi, Takashi Nomura,