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10.4049/jimmunol.1501724 http://scihub22266oqcxt.onion/10.4049/jimmunol.1501724 C4761524!4761524!26792803     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2016 ; 196 (5): 2368-76 Nephropedia Template TP {{tp|p=26792803|t=2016. Epithelial control of gut-associated lymphoid tissue formation through p38?-dependent restraint of NF-?B signaling |pdf=|usr=}}{{26792803}} gab.com Text Epithelial control of gut-associated lymphoid tissue formation through p38 -dependent restraint of NF- B signaling JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26792803 #FOAvip The protein kinase p38? mediates cellular responses to environmental and endogenous cues that direct tissue homeostasis and immune responses. Studies of mice lacking p38? in several different cell types have demonstrated that p38? signaling is essential to maintaining the proliferation-differentiation balance in developing and steady-state tissues. The mechanisms underlying these roles involve cell-autonomous control of signaling and gene expression by p38?. Here we show that p38? regulates gut-associated lymphoid tissue (GALT) formation in a non-cell-autonomous manner. From an investigation of mice with intestinal epithelial cell-specific deletion of the p38? gene, we find that p38? serves to limit NF-?B signaling and thereby attenuate GALT-promoting chemokine expression in the intestinal epithelium. Loss of this regulation results in GALT hyperplasia and, in some animals, mucosa-associated B cell lymphoma. These anomalies occur independently of luminal microbial stimuli and are likely driven by direct epithelial-lymphoid interactions. Our study illustrates a novel p38?-dependent mechanism preventing excessive generation of epithelial-derived signals that drive lymphoid tissue overgrowth and malignancy. Twit Text FOAVip Epithelial control of gut-associated lymphoid tissue formation through p38 -dependent restraint of NF- B signaling ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26792803 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26792803 #FOAvip English Wikipedia <ref>{{Cite pmid|26792803}}</ref> Epithelial control of gut-associated lymphoid tissue formation through p38?-dependent restraint of NF-?B signaling #MMPMID26792803 Caballero-Franco C; Guma M; Choo MK; Sano Y; Enzler T; Karin M; Mizoguchi A; Park JM J Immunol 2016[Mar]; 196 (5): 2368-76 PMID26792803show ga The protein kinase p38? mediates cellular responses to environmental and endogenous cues that direct tissue homeostasis and immune responses. Studies of mice lacking p38? in several different cell types have demonstrated that p38? signaling is essential to maintaining the proliferation-differentiation balance in developing and steady-state tissues. The mechanisms underlying these roles involve cell-autonomous control of signaling and gene expression by p38?. Here we show that p38? regulates gut-associated lymphoid tissue (GALT) formation in a non-cell-autonomous manner. From an investigation of mice with intestinal epithelial cell-specific deletion of the p38? gene, we find that p38? serves to limit NF-?B signaling and thereby attenuate GALT-promoting chemokine expression in the intestinal epithelium. Loss of this regulation results in GALT hyperplasia and, in some animals, mucosa-associated B cell lymphoma. These anomalies occur independently of luminal microbial stimuli and are likely driven by direct epithelial-lymphoid interactions. Our study illustrates a novel p38?-dependent mechanism preventing excessive generation of epithelial-derived signals that drive lymphoid tissue overgrowth and malignancy. äEpithelial control of gut-associated lymphoid tissue formation through(epmc).pdf DeepDyve Pubget Overpricing