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The Src Family Kinase Fyn Mediates Signals Induced by TCR Antagonists¹

Qizhi Tang^*, Sumit K. Subudhi, Kammi J. Henriksen, Catherine G. Long, Franklin Vives^* and Jeffrey A. Bluestone^2,*

^* The Diabetes Center, University of California, San Francisco, CA 94143; and University of Chicago, Chicago, IL 60637

FcR nonbinding anti-CD3 mAbs elicit partial TCR signaling that leads to T cell unresponsiveness and tolerance in vivo. In this study, the membrane-proximal events that promote T cell inactivation by FcR nonbinding anti-CD3 mAbs were examined. In the context of FcR nonbinding anti-CD3, TCR complexes did not aggregate and failed to translocate into glycolipid-enriched membrane microdomains. Furthermore, FcR nonbinding anti-CD3 mAbs induced tyrosine phosphorylation of the Fyn substrate Cbl, but not the ZAP-70 substrate linker for activation of T cells. Overexpression of Fyn, but not Lck, restored the mitogenicity of FcR nonbinding anti-CD3 in primary T cells. Taken together, these results suggest that Fyn mediates the partial signaling induced by TCR antagonists.

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