Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1371/journal.pntd.0005861 http://scihub22266oqcxt.onion/10.1371/journal.pntd.0005861 C5578697!5578697 !28827803     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28827803 &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 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28827803 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+Negl+Trop+Dis 2017 ; 11 (8 ): e0005861 Nephropedia Template TP {{tp|p=28827803 |t=2017. Host regulation of liver fibroproliferative pathology during experimental schistosomiasis via interleukin-4 receptor alpha |pdf=|usr=}}{{28827803 }} gab.com Text Host regulation of liver fibroproliferative pathology during experimental schistosomiasis via interleukin-4 receptor alpha JO: PLoS Negl Trop Dis http://www.kidney.de/pget.php?&tw=1&pmid=28827803 #FOAvip Interleukin-4 receptor (IL-4R?) is critical for the initiation of type-2 immune responses and implicated in the pathogenesis of experimental schistosomiasis. IL-4R? mediated type-2 responses are critical for the control of pathology during acute schistosomiasis. However, type-2 responses tightly associate with fibrogranulomatous inflammation that drives host pathology during chronic schistosomiasis. To address such controversy on the role of IL-4R?, we generated a novel inducible IL-4R?-deficient mouse model that allows for temporal knockdown of il-4r? gene after oral administration of Tamoxifen. Interrupting IL-4R? mediated signaling during the acute phase impaired the development of protective type-2 immune responses, leading to rapid weight loss and premature death, confirming a protective role of IL-4R? during acute schistosomiasis. Conversely, IL-4R? removal at the chronic phase of schistosomiasis ameliorated the pathological fibro-granulomatous pathology and reversed liver scarification without affecting the host fitness. This amelioration of the morbidity was accompanied by a reduced Th2 response and increased frequencies of FoxP3+ Tregs and CD1dhiCD5+ Bregs. Collectively, these data demonstrate that IL-4R? mediated signaling has two opposing functions during experimental schistosomiasis depending on the stage of advancement of the disease and indicate that interrupting IL-4R? mediated signaling is a viable therapeutic strategy to ameliorate liver fibroproliferative pathology in diseases like chronic schistosomiasis. Twit Text FOAVip Host regulation of liver fibroproliferative pathology during experimental schistosomiasis via interleukin-4 receptor alpha ????PLoS Negl Trop Dis http://www.kidney.de/pget.php?&tw=1&pmid=28827803 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28827803 #FOAvip English Wikipedia <ref>{{Cite pmid|28827803 }}</ref> Host regulation of liver fibroproliferative pathology during experimental schistosomiasis via interleukin-4 receptor alpha #MMPMID28827803 Nono JK ; Ndlovu H ; Aziz NA ; Mpotje T ; Hlaka L ; Brombacher F PLoS Negl Trop Dis 2017[Aug]; 11 (8 ): e0005861 PMID28827803 show ga Interleukin-4 receptor (IL-4R?) is critical for the initiation of type-2 immune responses and implicated in the pathogenesis of experimental schistosomiasis. IL-4R? mediated type-2 responses are critical for the control of pathology during acute schistosomiasis. However, type-2 responses tightly associate with fibrogranulomatous inflammation that drives host pathology during chronic schistosomiasis. To address such controversy on the role of IL-4R?, we generated a novel inducible IL-4R?-deficient mouse model that allows for temporal knockdown of il-4r? gene after oral administration of Tamoxifen. Interrupting IL-4R? mediated signaling during the acute phase impaired the development of protective type-2 immune responses, leading to rapid weight loss and premature death, confirming a protective role of IL-4R? during acute schistosomiasis. Conversely, IL-4R? removal at the chronic phase of schistosomiasis ameliorated the pathological fibro-granulomatous pathology and reversed liver scarification without affecting the host fitness. This amelioration of the morbidity was accompanied by a reduced Th2 response and increased frequencies of FoxP3+ Tregs and CD1dhiCD5+ Bregs. Collectively, these data demonstrate that IL-4R? mediated signaling has two opposing functions during experimental schistosomiasis depending on the stage of advancement of the disease and indicate that interrupting IL-4R? mediated signaling is a viable therapeutic strategy to ameliorate liver fibroproliferative pathology in diseases like chronic schistosomiasis. |*Host-Parasite Interactions [MESH] |Acute Disease [MESH] |Animals [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Fibrosis [MESH] |Liver/*pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Receptors, Cell Surface/genetics/*immunology [MESH] |Schistosomiasis/genetics/*immunology [MESH]Host regulation of liver fibroproliferative pathology during experimen(epmc).pdf DeepDyve Pubget Overpricing