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10.4049/jimmunol.1202176 http://scihub22266oqcxt.onion/10.4049/jimmunol.1202176 C3529820!3529820!23180822     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2013 ; 190 (1): 88-96 Nephropedia Template TP {{tp|p=23180822|t=2013. TIM-3 Regulates Innate Immune Cells to Induce Fetomaternal Tolerance |pdf=|usr=}}{{23180822}} gab.com Text TIM-3 Regulates Innate Immune Cells to Induce Fetomaternal Tolerance JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23180822 #FOAvip TIM-3 is constitutively expressed on subsets of macrophages and dendritic cells. Its expression on other cells of the innate immune system and its role in fetomaternal tolerance has not yet been explored. Here we investigate the role of TIM-3 expressing innate immune cells in the regulation of tolerance at the fetomaternal interface (FMI) using an allogeneic mouse model of pregnancy. Blockade of TIM-3 results in accumulation of inflammatory granulocytes and macrophages at the utero-placental interface and up regulation of pro-inflammatory cytokines. Furthermore, TIM-3 blockade inhibits the phagocytic potential of uterine macrophages resulting in a build up of apoptotic bodies at the utero-placental interface that elicits a local immune response. In response to inflammatory cytokines, Ly-6ChiGneg M-MDSCs (monocytic myeloid derived suppressor cells) expressing iNOS and arginase 1 are induced. However, these suppressive cells fail to down-regulate the inflammatory cascade induced by inflammatory granulocytes (Ly-6Cint Ghi) and apoptotic cells; the increased production of IFN? and TNF? by inflammatory granulocytes leads to abrogation of tolerance at the fetomaternal interface and fetal rejection. These data highlight the interplay between cells of the innate immune system at the FMI and their influence on successful pregnancy in mice. Twit Text FOAVip TIM-3 Regulates Innate Immune Cells to Induce Fetomaternal Tolerance ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23180822 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23180822 #FOAvip English Wikipedia <ref>{{Cite pmid|23180822}}</ref> TIM-3 Regulates Innate Immune Cells to Induce Fetomaternal Tolerance #MMPMID23180822 Chabtini L; Mfarrej B; Mounayar M; Zhu B; Batal I; Dakle PJ; Smith BD; Boenisch O; Najafian N; Akiba H; Yagita H; Guleria I J Immunol 2013[Jan]; 190 (1): 88-96 PMID23180822show ga TIM-3 is constitutively expressed on subsets of macrophages and dendritic cells. Its expression on other cells of the innate immune system and its role in fetomaternal tolerance has not yet been explored. Here we investigate the role of TIM-3 expressing innate immune cells in the regulation of tolerance at the fetomaternal interface (FMI) using an allogeneic mouse model of pregnancy. Blockade of TIM-3 results in accumulation of inflammatory granulocytes and macrophages at the utero-placental interface and up regulation of pro-inflammatory cytokines. Furthermore, TIM-3 blockade inhibits the phagocytic potential of uterine macrophages resulting in a build up of apoptotic bodies at the utero-placental interface that elicits a local immune response. In response to inflammatory cytokines, Ly-6ChiGneg M-MDSCs (monocytic myeloid derived suppressor cells) expressing iNOS and arginase 1 are induced. However, these suppressive cells fail to down-regulate the inflammatory cascade induced by inflammatory granulocytes (Ly-6Cint Ghi) and apoptotic cells; the increased production of IFN? and TNF? by inflammatory granulocytes leads to abrogation of tolerance at the fetomaternal interface and fetal rejection. These data highlight the interplay between cells of the innate immune system at the FMI and their influence on successful pregnancy in mice. äTIM-3 Regulates Innate Immune Cells to Induce Fetomaternal Tolerance (epmc).pdf DeepDyve Pubget Overpricing