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Subunits1
,
* Center for Immunology and
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390; and Departments of
Medical Biophysics and
Immunology, Ontario Cancer Institute, University of Toronto, Ontario, Canada
The functional effects of altered peptide ligands on T cells is proposed to involve differential intracellular signaling mediated by the 21- and 23-kDa tyrosine-phosphorylated derivatives of the TCR 
subunit (p21 and p23). To understand the functional contribution of p21 and p23 to T cell development and T cell antagonism, we generated selected TCR transgenic mice maintained on the P14 
TCR transgenic line such that p23 or both p21 and p23 were selectively eliminated. Importantly, one line (YF1,2) retains the constitutively tyrosine-phosphorylated p21 in the complete absence of inducible p23. We determined that T cell development was uncoupled from p21 and/or p23. Using a series of agonist, weak agonist, and antagonist peptides, we analyzed the role of each of the phosphorylated forms of TCR on T cell activation and antagonism. In this study, we report that the proliferative responses of P14 T cells to agonist peptides and the inhibition of proliferation resulting from antagonist peptide treatments was functionally uncoupled from p21 and/or p23. These results suggest that the mechanism of T cell antagonism is independent of the two phosphorylated TCR derivatives.
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