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Paper Chase

TAP transcription and phosphatidylinositol linkage mutants are defective in activation through the T cell receptor.

Cell. Mar 11, 1988;52(5):665-74.
Yeh ET, Reiser H, Bamezai A, Rock KL.

Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115.

Abstract:

TAP is a phosphatidylinositol-anchored membrane protein that is involved in murine T lymphocyte activation. To determine the relationship between TAP and T cell receptor/CD3-mediated activation, we derived TAP expression mutants of a T-T hybridoma. Two phenotypically distinct classes of mutants were obtained. The first has a selective defect in the transcription of TAP, while the second has a defect in the biosynthesis of phosphatidylinositol-protein linkages. Both mutations affect antigen-stimulated, T cell receptor-mediated activation of the T-T hybrid. These variants have intact immune effector gene programs, as they are responsive to pharmacologic agents that mimic receptor signals. These findings support a role for phosphatidylinositol-linked cell-surface glycoproteins in physiologic T cell activation. Consistent with this interpretation, we observed similar defects in T cell responsiveness after enzymatic removal of phosphatidylinositol-linked proteins from normal T lymphocytes.