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10.1182/blood-2016-05-719757 http://scihub22266oqcxt.onion/10.1182/blood-2016-05-719757 C5095756!5095756 !27683415     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 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\27683415 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Blood 2016 ; 128 (18 ): 2218-2228 Nephropedia Template TP {{tp|p=27683415 |t=2016. C1q and HMGB1 reciprocally regulate human macrophage polarization |pdf=|usr=}}{{27683415 }} gab.com Text C1q and HMGB1 reciprocally regulate human macrophage polarization JO: Blood http://www.kidney.de/pget.php?&tw=1&pmid=27683415 #FOAvip A healthy immune system results from a balance of stimulatory and inhibitory pathways that allow effective responses to acute insults, without descending into chronic inflammation. Failed homeostasis is characteristic of autoimmune diseases such as systemic lupus erythematosus. Although HMGB1 induces proinflammatory M1-like macrophage differentiation, we describe a mechanism by which C1q modulates this activity and collaborates with HMGB1 to induce the differentiation of monocytes to anti-inflammatory M2-like macrophages. These anti-inflammatory macrophages are unresponsive to dendritic cell induction factors, effectively removing them from participation in an adaptive immune response. This pathway is mediated through a complex with RAGE and LAIR-1 and depends on relative levels of C1q and HMGB1. Importantly, these data provide insight into a homeostatic mechanism in which C1q and HMGB1 can cooperate to terminate inflammation, and which may be impaired in C1q-deficient patients with autoimmune disease. Twit Text FOAVip C1q and HMGB1 reciprocally regulate human macrophage polarization ????Blood http://www.kidney.de/pget.php?&tw=1&pmid=27683415 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27683415 #FOAvip English Wikipedia <ref>{{Cite pmid|27683415 }}</ref> C1q and HMGB1 reciprocally regulate human macrophage polarization #MMPMID27683415 Son M ; Porat A ; He M ; Suurmond J ; Santiago-Schwarz F ; Andersson U ; Coleman TR ; Volpe BT ; Tracey KJ ; Al-Abed Y ; Diamond B Blood 2016[Nov]; 128 (18 ): 2218-2228 PMID27683415 show ga A healthy immune system results from a balance of stimulatory and inhibitory pathways that allow effective responses to acute insults, without descending into chronic inflammation. Failed homeostasis is characteristic of autoimmune diseases such as systemic lupus erythematosus. Although HMGB1 induces proinflammatory M1-like macrophage differentiation, we describe a mechanism by which C1q modulates this activity and collaborates with HMGB1 to induce the differentiation of monocytes to anti-inflammatory M2-like macrophages. These anti-inflammatory macrophages are unresponsive to dendritic cell induction factors, effectively removing them from participation in an adaptive immune response. This pathway is mediated through a complex with RAGE and LAIR-1 and depends on relative levels of C1q and HMGB1. Importantly, these data provide insight into a homeostatic mechanism in which C1q and HMGB1 can cooperate to terminate inflammation, and which may be impaired in C1q-deficient patients with autoimmune disease. |Cell Differentiation/*immunology [MESH] |Cell Polarity [MESH] |Complement C1q/immunology/*metabolism [MESH] |HMGB1 Protein/immunology/*metabolism [MESH] |Humans [MESH] |Macrophages/*cytology/immunology/metabolism [MESH]C1q and HMGB1 reciprocally regulate human macrophage polarization (epmc).pdf DeepDyve Pubget Overpricing