作者: J. B. Swann , M. D. Vesely , A. Silva , J. Sharkey , S. Akira
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摘要: Here we report the effects of loss Toll-like receptor-associated signaling adaptor myeloid-differentiation factor 88 (MyD88) on tumor induction in two distinct mouse models carcinogenesis. The 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol 13-acetate (TPA)-induced skin papilloma model depends proinflammatory processes, whereas 3′-methylcholanthrene (MCA) fibrosarcoma has been used by immunologists to illustrate innate and adaptive immune surveillance cancer. When exposed a combination DMBA/TPA, mice lacking MyD88 formed fewer papillomas than genetically matched WT controls treated similar manner. Unexpectedly, however, MyD88−/− sarcomas when MCA. In contrast, MyD88-deficient did not show defective ability reject highly immunogenic transplanted tumors, including MCA sarcomas. Despite reported role TNF chronic inflammation, TNF-deficient were significantly more susceptible MCA-induced sarcoma mice. Overall, these data only confirm key that plays promoting development but also demonstrate inflammation-induced carcinogenesis cancer immunoediting can indeed occur same model.