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Cutting Edge: Dependence of TCR Antagonism on Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase Activity¹

Neely E. Kilgore^*, Jenny D. Carter, Ulrike Lorenz and Brian D. Evavold^2,*

^* Department of Microbiology and Immunology, Emory University, Atlanta, GA 30322; and Department of Microbiology, University of Virginia Health Sciences Center, Charlottesville, VA 22908

The mechanism by which antagonist peptides inhibit T cell responses is unknown. Mice deficient in Src homology 2 domain-containing protein tyrosine phosphatase (SHP-1) have revealed its importance in the negative regulation of lymphocyte signaling. We investigated a possible role for SHP-1 in T cell antagonism and demonstrate, for the first time, a substantial increase in SHP-1 activity during antagonism of CD4⁺ T cells. Furthermore, the removal of functional SHP-1 prevents antagonism in these cells. Our data demonstrate that T cell antagonism occurs via a negative intracellular signal that is mediated by SHP-1.

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