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Subunit and Syk Kinase Replace the CD3
-Chain and ZAP-70 Kinase in the TCR Signaling Complex of Human Effector CD4 T Cells1
,
,
* Departments of Surgery, and Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201;
Department of Cellular Injury, Walter Reed Army Institute of Research, Silver Spring, MD 20910; and
Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814
The TCR-mediated signals required to activate resting T cells have been well characterized; however, it is not known how TCR-coupled signals are transduced in differentiated effector T cells that coordinate ongoing immune responses. Here we demonstrate that human effector CD4 T cells up-regulate the expression of the CD3
-related FcR
signaling subunit that becomes part of an altered TCR/CD3 signaling complex containing CD3
, but not CD3. The TCR/CD3/FcR complex in effector cells recruits and activates the Syk, but not the ZAP-70, tyrosine kinase. This physiologic switch in TCR signaling occurs exclusively in effector, and not naive or memory T cells, suggesting a potential target for manipulation of effector responses in autoimmune, malignant, and infectious diseases.
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