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.

10.1182/bloodadvances.2017012187 http://scihub22266oqcxt.onion/10.1182/bloodadvances.2017012187 C5873231!5873231 !29563123     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29563123 &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 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 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\29563123 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Blood+Adv 2018 ; 2 (6 ): 669-680 Nephropedia Template TP {{tp|p=29563123 |t=2018. Murine CMV induces type 1 IFN that impairs differentiation of MDSCs critical for transplantation tolerance |pdf=|usr=}}{{29563123 }} gab.com Text Murine CMV induces type 1 IFN that impairs differentiation of MDSCs critical for transplantation tolerance JO: Blood Adv http://www.kidney.de/pget.php?&tw=1&pmid=29563123 #FOAvip Clinical tolerance without immunosuppression has now been achieved for organ transplantation, and its scope will likely continue to expand. In this context, a previously understudied and now increasingly relevant area is how microbial infections might affect the efficacy of tolerance. A highly prevalent and clinically relevant posttransplant pathogen is cytomegalovirus (CMV). Its impact on transplantation tolerance and graft outcomes is not well defined. Employing a mouse model of CMV (MCMV) infection and allogeneic pancreatic islet transplantation in which donor-specific tolerance was induced by infusing donor splenocytes rendered apoptotic by treatment with ethylenecarbodiimide, we investigated the effect of CMV infection on transplantation tolerance induction. We found that acute MCMV infection abrogated tolerance induction and that this abrogation correlated with an alteration in the differentiation and function of myeloid-derived suppressor cells (MDSCs). These effects on MDSCs were mediated in part through MCMV induced type 1 interferon (IFN) production. During MCMV infection, the highly immunosuppressive Gr1(HI)-granulocytic MDSCs were markedly reduced in numbers, and the accumulating Ly6C(HI)-monocytic cells lost their MDSC-like function but instead acquired an immunostimulatory phenotype to cross-present alloantigens and prime alloreactive CD8 T cells. Consequently, the islet allograft exhibited an altered effector to regulatory T-cell ratio that correlated with the ultimate graft demise. Blocking type 1 IFN signaling during MCMV infection rescued MDSC populations and partially restored transplantation tolerance. Our mechanistic studies now provide a solid foundation for seeking effective therapies for promoting transplantation tolerance in settings of CMV infection. Twit Text FOAVip Murine CMV induces type 1 IFN that impairs differentiation of MDSCs critical for transplantation tolerance ????Blood Adv http://www.kidney.de/pget.php?&tw=1&pmid=29563123 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29563123 #FOAvip English Wikipedia <ref>{{Cite pmid|29563123 }}</ref> Murine CMV induces type 1 IFN that impairs differentiation of MDSCs critical for transplantation tolerance #MMPMID29563123 Dangi A ; Zhang L ; Zhang X ; Luo X Blood Adv 2018[Mar]; 2 (6 ): 669-680 PMID29563123 show ga Clinical tolerance without immunosuppression has now been achieved for organ transplantation, and its scope will likely continue to expand. In this context, a previously understudied and now increasingly relevant area is how microbial infections might affect the efficacy of tolerance. A highly prevalent and clinically relevant posttransplant pathogen is cytomegalovirus (CMV). Its impact on transplantation tolerance and graft outcomes is not well defined. Employing a mouse model of CMV (MCMV) infection and allogeneic pancreatic islet transplantation in which donor-specific tolerance was induced by infusing donor splenocytes rendered apoptotic by treatment with ethylenecarbodiimide, we investigated the effect of CMV infection on transplantation tolerance induction. We found that acute MCMV infection abrogated tolerance induction and that this abrogation correlated with an alteration in the differentiation and function of myeloid-derived suppressor cells (MDSCs). These effects on MDSCs were mediated in part through MCMV induced type 1 interferon (IFN) production. During MCMV infection, the highly immunosuppressive Gr1(HI)-granulocytic MDSCs were markedly reduced in numbers, and the accumulating Ly6C(HI)-monocytic cells lost their MDSC-like function but instead acquired an immunostimulatory phenotype to cross-present alloantigens and prime alloreactive CD8 T cells. Consequently, the islet allograft exhibited an altered effector to regulatory T-cell ratio that correlated with the ultimate graft demise. Blocking type 1 IFN signaling during MCMV infection rescued MDSC populations and partially restored transplantation tolerance. Our mechanistic studies now provide a solid foundation for seeking effective therapies for promoting transplantation tolerance in settings of CMV infection. |*Transplantation Tolerance [MESH] |Animals [MESH] |Apoptosis/immunology [MESH] |Biomarkers [MESH] |Cell Differentiation [MESH] |Cell Lineage [MESH] |Herpesviridae Infections/immunology/*metabolism/*virology [MESH] |Immunomodulation/genetics/immunology [MESH] |Inflammation Mediators/metabolism [MESH] |Interferon Type I/*metabolism [MESH] |Islets of Langerhans/immunology/metabolism [MESH] |Male [MESH] |Mice [MESH] |Monocytes/immunology/metabolism [MESH] |Muromegalovirus/*physiology [MESH] |Myeloid-Derived Suppressor Cells/cytology/*immunology/*metabolism/virology [MESH] |T-Lymphocyte Subsets/immunology/metabolism [MESH]Murine CMV induces type 1 IFN that impairs differentiation of MDSCs cr(epmc).pdf DeepDyve Pubget Overpricing