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International Immunology, Vol. 13, No. 8, 1085-1093, August 2001
© 2001 Japanese Society for Immunology

Altered functional and biochemical response by CD8+ T cells that remain after tolerance

Anwar Murtaza, C. Thomas Nugent2, Pankaj Tailor3, Valerie C. Asensio1, Judith A. Biggs, Iain L. Campbell1 and Linda A. Sherman

1 Departments of Immunology and Neuropharmacology, The Scripps Research Institute, 10550 North Torrey Pines Road, IMM-15, La Jolla, CA 92037, USA
2 Hybritech Inc., a subsidiary of Beckman Coulter Inc., PO Box 269006, San Diego, CA 92196, USA
3 Department of Biochemistry, Room 904, McIntyre Medical Building, 3655 Drummond Street, McGill University, Montreal, Quebec H3G 1Y6, Canada

Correspondence to: L A. Sherman

To further define the molecular basis of tolerance to a peripherally expressed antigen we have correlated differences in functional capacity with biochemical events in hemagglutinin (HA)-specific cytotoxic T lymphocyte (CTL) clones derived either from a conventional B10.D2 mouse that is not tolerant to HA (D2 Clone 6) or from an InsHA mouse that is tolerant to HA (InsHA Clone 12). D2 Clone 6, but not InsHA Clone 12, triggers diabetes following in vivo transfer into irradiated InsHA hosts. This diabetogenic clone shows complete and sustained phosphorylation of TCR {zeta}{zeta} chain and ZAP-70 following stimulation with HA-pulsed antigen-presenting cells. In contrast, InsHA Clone 12 showed only partial phosphorylation of TCR {zeta}{zeta} and no phosphorylation of ZAP-70. There was no defect in activation or recruitment of Lck to the TCR complex in both the clones following stimulation with the cognate antigen. This deficiency in the proximal signaling in the InsHA Clone 12 could be overcome by increasing the strength of signal through the CD3–TCR complex, indicating that the signaling machinery of InsHA Clone 12 was functional. These data demonstrate that the HA-responsive CD8+ T cells that can be retrieved from InsHA mice after tolerance induction respond to HA as a partial agonist/antagonist.

Keywords: diabetes, signal transduction, TCR, tolerance

Transmitting editor: S. L. Swain


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