期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 117, 期 5, 页码 1167-1174出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI31202
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资金
- NCI NIH HHS [CA 100425, R01 CA100425, CA 105207, R01 CA105207] Funding Source: Medline
- FDA HHS [FD 003118, R01 FD003118] Funding Source: Medline
Tumors express antigens that should induce immune-mediated rejection, but spontaneous rejection of established tumors is rare. Recent work demonstrates actively defeat host immunity. This concept forces us to rethink current approaches to harnessing potent, specific host immunity to battle cancer, most of which are based on the paradigm that inducing more antitumor immune cells alone is therapeutic. However, as I discuss in this Personal Perspective, a newer paradigm predicts that reducing tumor-driven immune suppression will be clinically beneficial. CD4(+)CD25(+) Tregs are one mechanism of tumor-driven immune evasion that provide prototypical targets for testing novel anticancer treatment strategies within the newer paradigm.
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