Journal
JOURNAL OF IMMUNOLOGY
Volume 170, Issue 8, Pages 4189-4195Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.170.8.4189
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Funding
- NIAID NIH HHS [AI42092, R01AI42269] Funding Source: Medline
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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 CD3zeta-related FcRgamma signaling subunit that becomes part of an altered TCR/CD3 signaling complex containing CD3is an element of, but not CDzeta3. The TCR/CD3/FcRgamma 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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