期刊
CANCER IMMUNOLOGY RESEARCH
卷 2, 期 5, 页码 410-422出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2326-6066.CIR-13-0171
关键词
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资金
- U.S. NIH [R01AI081848, R01AI071078, R43CA153669]
- Melanoma Research Alliance
- Cancer Research Institute
- Programme for Advanced Medical Education
- ACS grant [RSG-11-057-01-LIB]
- NIH [R01 NS045937, P01 AI07378]
- NYU Cancer Institute NCI Cancer Center Support Grant [5 P30 CA 016087-27]
- Marc Jacobs Campaign
The immunoregulatory protein T-cell immunoglobulin-and mucin-domain-containing molecule-3 (Tim-3) mediates T-cell exhaustion and contributes to the suppression of immune responses in both viral infections and tumors. Tim-3 blockade reverses the exhausted phenotype of CD4(+) and CD8(+) T cells in several chronic diseases, including melanoma. Interestingly, natural killer (NK) cells constitutively express Tim-3; however, the role of Tim-3 in modulating the function of these innate effector cells remains unclear, particularly in human diseases. In this study, we compared the function of Tim-3 in NK cells from healthy donors and patients with metastatic melanoma. NK cells from the latter were functionally impaired/exhausted, and Tim-3 blockade reversed this exhausted phenotype. Moreover, Tim-3 expression levels were correlated with the stage of the disease and poor prognostic factors. These data indicate that Tim-3 can function as an NK-cell exhaustion marker in advanced melanoma and support the development of Tim-3-targeted therapies to restore antitumor immunity. (C) 2014 AACR.
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