کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4359874 1301117 2013 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
MyD88 and its divergent toll in carcinogenesis
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
MyD88 and its divergent toll in carcinogenesis
چکیده انگلیسی


• MyD88 contributes to carcinogenesis in experimental models.
• MyD88 promotes tumor formation through its role in cancer-associated inflammation.
• Through its involvement in tissue repair, MyD88 can also protect against tumor formation.
• MyD88-dependent adaptive immune responses protect against oncogenic pathogens.

Toll-like and interleukin-1 (IL-1) family receptors recognize microbial or endogenous ligands and inflammatory mediators, respectively, and with the exception of Toll-like receptor 3 (TLR3), signal via the adaptor molecule myeloid differentiation factor 88 (MyD88). MyD88 is involved in oncogene-induced cell intrinsic inflammation and in cancer-associated extrinsic inflammation, and as such MyD88 contributes to skin, liver, pancreatic, and colon carcinogenesis, as well as sarcomagenesis. MyD88 is also protective, for example in oncogenic virus carcinogenesis or, acting downstream of IL-18R to strengthen mucosal repair, in azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colon carcinogenesis. Here, we discuss the mechanisms of the divergent effects of MyD88 and the balance of its protumor role in cancer-enhancing inflammation and immunity and its antitumor role in tissue homeostasis, repair, and immunity against the tumor or oncogenic pathogens.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 34, Issue 8, August 2013, Pages 379–389
نویسندگان
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