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10.4049/jimmunol.1302771 http://scihub22266oqcxt.onion/10.4049/jimmunol.1302771 C4082999!4082999 !24808363     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24808363 &cmd=llinks): Failed to open stream: HTTP request failed! 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Preemptive donor apoptotic cell infusions induce IFN-?-producing myeloid-derived suppressor cells for cardiac allograft protection |pdf=|usr=}}{{24808363 }} gab.com Text Preemptive donor apoptotic cell infusions induce IFN- -producing myeloid-derived suppressor cells for cardiac allograft protection JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24808363 #FOAvip We have previously shown that preemptive infusion of apoptotic donor splenocytes treated with the chemical cross-linker ethylcarbodiimide (ECDI-SPs) induces long-term allograft survival in full MHC-mismatched models of allogeneic islet and cardiac transplantation. The role of myeloid-derived suppressor cells (MDSCs) in the graft protection provided by ECDI-SPs is unclear. In this study, we demonstrate that infusions of ECDI-SPs increase two populations of CD11b(+) cells in the spleen that phenotypically resemble monocytic-like (CD11b(+)Ly6C(high)) and granulocytic-like (CD11b(+)Gr1(high)) MDSCs. Both populations suppress T cell proliferation in vitro and traffic to the cardiac allografts in vivo to mediate their protection via inhibition of local CD8 T cell accumulation and potentially also via induction and homing of regulatory T cells. Importantly, repeated treatments with ECDI-SPs induce the CD11b(+)Gr1(high) cells to produce a high level of IFN-? and to exhibit an enhanced responsiveness to IFN-? by expressing higher levels of downstream effector molecules ido and nos2. Consequently, neutralization of IFN-? completely abolishes the suppressive capacity of this population. We conclude that donor ECDI-SPs induce the expansion of two populations of MDSCs important for allograft protection mediated in part by intrinsic IFN-?-dependent mechanisms. This form of preemptive donor apoptotic cell infusions has significant potential for the therapeutic manipulation of MDSCs for transplant tolerance induction. Twit Text FOAVip Preemptive donor apoptotic cell infusions induce IFN- -producing myeloid-derived suppressor cells for cardiac allograft protection ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24808363 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24808363 #FOAvip English Wikipedia <ref>{{Cite pmid|24808363 }}</ref> Preemptive donor apoptotic cell infusions induce IFN-?-producing myeloid-derived suppressor cells for cardiac allograft protection #MMPMID24808363 Bryant J ; Lerret NM ; Wang JJ ; Kang HK ; Tasch J ; Zhang Z ; Luo X J Immunol 2014[Jun]; 192 (12 ): 6092-101 PMID24808363 show ga We have previously shown that preemptive infusion of apoptotic donor splenocytes treated with the chemical cross-linker ethylcarbodiimide (ECDI-SPs) induces long-term allograft survival in full MHC-mismatched models of allogeneic islet and cardiac transplantation. The role of myeloid-derived suppressor cells (MDSCs) in the graft protection provided by ECDI-SPs is unclear. In this study, we demonstrate that infusions of ECDI-SPs increase two populations of CD11b(+) cells in the spleen that phenotypically resemble monocytic-like (CD11b(+)Ly6C(high)) and granulocytic-like (CD11b(+)Gr1(high)) MDSCs. Both populations suppress T cell proliferation in vitro and traffic to the cardiac allografts in vivo to mediate their protection via inhibition of local CD8 T cell accumulation and potentially also via induction and homing of regulatory T cells. Importantly, repeated treatments with ECDI-SPs induce the CD11b(+)Gr1(high) cells to produce a high level of IFN-? and to exhibit an enhanced responsiveness to IFN-? by expressing higher levels of downstream effector molecules ido and nos2. Consequently, neutralization of IFN-? completely abolishes the suppressive capacity of this population. We conclude that donor ECDI-SPs induce the expansion of two populations of MDSCs important for allograft protection mediated in part by intrinsic IFN-?-dependent mechanisms. This form of preemptive donor apoptotic cell infusions has significant potential for the therapeutic manipulation of MDSCs for transplant tolerance induction. |*Apoptosis [MESH] |*Heart Transplantation [MESH] |Allografts [MESH] |Animals [MESH] |Graft Survival/*immunology [MESH] |Interferon-gamma/*immunology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Myeloid Cells/*immunology [MESH]Preemptive donor apoptotic cell infusions induce IFN-?-producing myelo(epmc).pdf DeepDyve Pubget Overpricing