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The Journal of Immunology, Vol 155, Issue 11 5083-5087, Copyright © 1995 by American Association of Immunologists

CUTTING EDGE

Defective TCR-mediated signaling in anergic T cells [published erratum appears in J Immunol 1996 Apr 15;156(8):following 3088]

K Migita, K Eguchi, Y Kawabe, T Tsukada, Y Ichinose, S Nagataki and A Ochi
First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

Extrathymic T cell tolerance to Ags can be achieved through clonal deletion by activation-induced programmed cell death as well as by functional unresponsiveness (anergy) of Ag reactive-T cells. Previous studies demonstrated that in vivo administration of staphylococcal enterotoxin B (SEB) induces SEB-specific T cell anergy. To investigate the molecular mechanisms of T cell anergy, we analyzed the TCR-mediated signal transduction in normal and anergic T cells. Anergic T cells exhibited impaired protein tyrosine phosphorylation on TCR-mediated stimulation. The altered tyrosine phosphorylation in anergic T cells may be caused by a defect in tyrosine phosphorylation of TCR zeta-chain and its subsequent association with ZAP-70 tyrosine kinase. Our data demonstrated that TCR zeta-chain phosphorylation and its sequential interaction with ZAP-70 are essential for the initiation of TCR- mediated signal transduction.


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