Abstract

The localization of γδ T cells within epithelia suggests that these cells may contribute to the down-regulation of epithelial malignancies. We report that mice lacking γδ 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 + γδ 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.

Keywords

NKG2DCytolysisBiologyMalignancyMajor histocompatibility complexCarcinogenesisIn vitroCarcinogenCancer researchReceptorImmunologyCell biologyAntigenCytotoxicityCancerGenetics

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Publication Info

Year
2001
Type
article
Volume
294
Issue
5542
Pages
605-609
Citations
957
Access
Closed

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Cite This

Michael Girardi, David Oppenheim, Carrie R. Steele et al. (2001). Regulation of Cutaneous Malignancy by γδ T Cells. Science , 294 (5542) , 605-609. https://doi.org/10.1126/science.1063916

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DOI
10.1126/science.1063916