
The localization of gammadelta T cells within epithelia suggests that these cells may contribute to the down-regulation of epithelial malignancies. We report that mice lacking gammadelta cells are highly susceptible to multiple regimens of cutaneous carcinogenesis. After exposure to carcinogens, skin cells expressed Rae-1 and H60, major histocompatibility complex-related molecules structurally resembling human MICA. Each of these is a ligand for NKG2d, a receptor expressed by cytolytic T cells and natural killer (NK) cells. In vitro, skin-associated NKG2d+ gammadelta cells killed skin carcinoma cells by a mechanism that was sensitive to blocking NKG2d engagement. Thus, local T cells may use evolutionarily conserved proteins to negatively regulate malignancy.
Cytotoxicity, Immunologic, Protein Folding, Protein Conformation, Histocompatibility Antigens Class I, Molecular Sequence Data, 610, Membrane Proteins, Epithelial Cells, Ligands, Cell Line, Mice, Inbred C57BL, Minor Histocompatibility Antigens, Mice, NK Cell Lectin-Like Receptor Subfamily K, 616, Carcinogens, Animals, Humans, Amino Acid Sequence, Epidermis, Dimerization, Immunologic Surveillance
Cytotoxicity, Immunologic, Protein Folding, Protein Conformation, Histocompatibility Antigens Class I, Molecular Sequence Data, 610, Membrane Proteins, Epithelial Cells, Ligands, Cell Line, Mice, Inbred C57BL, Minor Histocompatibility Antigens, Mice, NK Cell Lectin-Like Receptor Subfamily K, 616, Carcinogens, Animals, Humans, Amino Acid Sequence, Epidermis, Dimerization, Immunologic Surveillance
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