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CD8 +  tumor infiltrating T cells (TIL) lack effector-phase functions due to defective proximal TCR-mediated signaling previously shown to result from inactivation of p56 lck  kinase. We identify a novel interacting partner for p56 lck  in nonlytic TIL, Protocadherin-18 (‘pcdh18’), and show that pcdh18 is transcribed upon  in vitro  or  in vivo  activation of all CD8 +  central memory T cells (CD44 + CD62L hi CD127 + ) coincident with conversion into effector memory cells (CD44 + CD62L lo CD127 + ). Expression of pcdh18 in primary CD8 +  effector cells induces the phenotype of nonlytic TIL: defective proximal TCR signaling, cytokine secretion, and cytolysis, and enhanced AICD. pcdh18 contains a motif (centered at Y842) shared with src kinases (QGQYQP) that is required for the inhibitory phenotype. Thus, pcdh18 is a novel activation marker of CD8 +  memory T cells that can function as an inhibitory signaling receptor and restrict the effector phase.

Protocadherin-18 Is a Novel Differentiation Marker and an Inhibitory Signaling Receptor for CD8+ Effector Memory T Cells