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10.4049/jimmunol.1602056 http://scihub22266oqcxt.onion/10.4049/jimmunol.1602056 C5531203!5531203!28630091     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28630091&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2017 ; 199 (2): 750-60 Nephropedia Template TP {{tp|p=28630091|t=2017. B-1a Cells Protect Mice from Sepsis: Critical Role of cAMP-response Element Binding Protein (CREB) |pdf=|usr=}}{{28630091}} gab.com Text B-1a Cells Protect Mice from Sepsis: Critical Role of cAMP-response Element Binding Protein (CREB) JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28630091 #FOAvip Bacterial sepsis is a serious life-threatening condition caused by an excessive immune response to infection. B-1 cells differ from conventional B-2 cells by their distinct phenotype and function. A subset of B-1 cells expressing CD5, known as B-1a cells, exhibits innate immune activity. Here we report that B-1a cells play a beneficial role in sepsis by mitigating exaggerated inflammation through a novel mechanism. Using a mouse model of bacterial sepsis, we found that the numbers of B-1a cells in various anatomical locations were significantly decreased. Adoptive transfer of B-1a cells into septic mice significantly attenuated systemic inflammation and improved survival, while B-1a cell deficient CD19-/- mice were more susceptible to infectious inflammation and mortality. We also demonstrated B-1a cells produced ample amounts of IL-10 which controlled excessive inflammation and the mice treated with IL-10 deficient B-1a cells were not protected against sepsis. Moreover, we identified a novel intracellular signaling molecule cAMP-response element binding protein (CREB) which serves as a pivotal transcription factor for up-regulating IL-10 production by B-1a cells in sepsis through its nuclear translocation and binding to putative responsive elements on IL-10 promoter. Thus, the benefit of B-1a cells in bacterial sepsis is mediated by CREB and the identification of CREB in B-1a cells reveals a potential avenue for treatment in bacterial sepsis. Twit Text FOAVip B-1a Cells Protect Mice from Sepsis: Critical Role of cAMP-response Element Binding Protein (CREB) ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28630091 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28630091 #FOAvip English Wikipedia <ref>{{Cite pmid|28630091}}</ref> B-1a Cells Protect Mice from Sepsis: Critical Role of cAMP-response Element Binding Protein (CREB) #MMPMID28630091 Aziz M; Holodick NE; Rothstein TL; Wang P J Immunol 2017[Jul]; 199 (2): 750-60 PMID28630091show ga Bacterial sepsis is a serious life-threatening condition caused by an excessive immune response to infection. B-1 cells differ from conventional B-2 cells by their distinct phenotype and function. A subset of B-1 cells expressing CD5, known as B-1a cells, exhibits innate immune activity. Here we report that B-1a cells play a beneficial role in sepsis by mitigating exaggerated inflammation through a novel mechanism. Using a mouse model of bacterial sepsis, we found that the numbers of B-1a cells in various anatomical locations were significantly decreased. Adoptive transfer of B-1a cells into septic mice significantly attenuated systemic inflammation and improved survival, while B-1a cell deficient CD19-/- mice were more susceptible to infectious inflammation and mortality. We also demonstrated B-1a cells produced ample amounts of IL-10 which controlled excessive inflammation and the mice treated with IL-10 deficient B-1a cells were not protected against sepsis. Moreover, we identified a novel intracellular signaling molecule cAMP-response element binding protein (CREB) which serves as a pivotal transcription factor for up-regulating IL-10 production by B-1a cells in sepsis through its nuclear translocation and binding to putative responsive elements on IL-10 promoter. Thus, the benefit of B-1a cells in bacterial sepsis is mediated by CREB and the identification of CREB in B-1a cells reveals a potential avenue for treatment in bacterial sepsis. äB-1a Cells Protect Mice from Sepsis: Critical Role of cAMP-response El(epmc).pdf DeepDyve Pubget Overpricing