27
November 2003
Rheumatoid arthritis: T-cell defect
Normal T-cell development in the thymus involves the elimination of self-reactive T-cell clones. Autoimmune T cells are prime mediators of rheumatoid arthritis, so this self-policing step is a prime suspect in the search for the cause of the disease. Identification of a point mutation in mice as the cause of a condition very like rheumatoid arthritis now provides direct evidence linking altered T-cell selection to an arthritic disease. The mutation in the signalling molecule ZAP-70 skews T-cell selection to favour preservation of autoimmune cells. Rheumatoid arthritis is a complex disease so this point mutation is not the end of the story. But it could help in the development of methods for the detection, treatment and prevention of autoimmune arthritis.
Altered thymic T-cell selection due to a mutation
of the ZAP-70 gene causes autoimmune arthritis in mice
NORIKO SAKAGUCHI , TAKESHI TAKAHASHI, HIROSHI HATA,
TAKASHI NOMURA, TOMOYUKI TAGAMI, SAYURI YAMAZAKI, TOSHIKO SAKIHAMA, TAKAJI
MATSUTANI, IZUMI NEGISHI, SYUICHI NAKATSURU & SHIMON SAKAGUCHI
Nature 426, 454–460 (2003); doi:10.1038/nature02119
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