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10.1002/ijc.24923 http://scihub22266oqcxt.onion/10.1002/ijc.24923 C4068029!4068029!19795459     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Cancer 2010 ; 126 (7): 1651-65 Nephropedia Template TP {{tp|p=19795459|t=2010. Unifying roles for regulatory T cells and inflammation in cancer |pdf=|usr=}}{{19795459}} gab.com Text Unifying roles for regulatory T cells and inflammation in cancer JO: Int J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=19795459 #FOAvip Activities of CD4+ regulatory (TREG) cells restore immune homeostasis during chronic inflammatory disorders. Roles for TREG cells in inflammation-associated cancers, however, are paradoxical. It is widely believed that TREG function in cancer mainly to suppress protective anticancer responses. However, we demonstrate here that TREG cells also function to reduce cancer risk throughout the body by efficiently downregulating inflammation arising from the gastrointestinal (GI) tract. Building on a ?hygiene hypothesis? model in which GI infections lead to changes in TREG that reduce immune-mediated diseases, here we show that gut bacteria-triggered TREG may function to inhibit cancer even in extraintestinal sites. Ability of bacteria-stimulated TREG to suppress cancer depends on interleukin (IL)-10, which serves to maintain immune homeostasis within bowel and support a protective antiinflammatory TREG phenotype. However, under proinflammatory conditions, TREG may fail to provide antiinflammatory protection and instead contribute to a T helper (Th)-17-driven procarcinogenic process; a cancer state that is reversible by downregulation of inflammation. Consequently, hygienic individuals with a weakened IL-10 and TREG-mediated inhibitory loop are highly susceptible to the carcinogenic consequences of elevated IL-6 and IL-17 and show more frequent inflammation-associated cancers. Taken together, these data unify seemingly divergent disease processes such as autoimmunity and cancer and help explain the paradox of TREG and inflammation in cancer. Enhancing protective TREG functions may promote healthful longevity and significantly reduce risk of cancer. Twit Text FOAVip Unifying roles for regulatory T cells and inflammation in cancer ????Int J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=19795459 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19795459 #FOAvip English Wikipedia <ref>{{Cite pmid|19795459}}</ref> Unifying roles for regulatory T cells and inflammation in cancer #MMPMID19795459 Erdman SE; Rao VP; Olipitz W; Taylor CL; Jackson EA; Levkovich T; Lee CW; Horwitz BH; Fox JG; Ge Z; Poutahidis T Int J Cancer 2010[Apr]; 126 (7): 1651-65 PMID19795459show ga Activities of CD4+ regulatory (TREG) cells restore immune homeostasis during chronic inflammatory disorders. Roles for TREG cells in inflammation-associated cancers, however, are paradoxical. It is widely believed that TREG function in cancer mainly to suppress protective anticancer responses. However, we demonstrate here that TREG cells also function to reduce cancer risk throughout the body by efficiently downregulating inflammation arising from the gastrointestinal (GI) tract. Building on a ?hygiene hypothesis? model in which GI infections lead to changes in TREG that reduce immune-mediated diseases, here we show that gut bacteria-triggered TREG may function to inhibit cancer even in extraintestinal sites. Ability of bacteria-stimulated TREG to suppress cancer depends on interleukin (IL)-10, which serves to maintain immune homeostasis within bowel and support a protective antiinflammatory TREG phenotype. However, under proinflammatory conditions, TREG may fail to provide antiinflammatory protection and instead contribute to a T helper (Th)-17-driven procarcinogenic process; a cancer state that is reversible by downregulation of inflammation. Consequently, hygienic individuals with a weakened IL-10 and TREG-mediated inhibitory loop are highly susceptible to the carcinogenic consequences of elevated IL-6 and IL-17 and show more frequent inflammation-associated cancers. Taken together, these data unify seemingly divergent disease processes such as autoimmunity and cancer and help explain the paradox of TREG and inflammation in cancer. Enhancing protective TREG functions may promote healthful longevity and significantly reduce risk of cancer. äUnifying roles for regulatory T cells and inflammation in cancer (epmc).pdf DeepDyve Pubget Overpricing