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10.3389/fimmu.2020.595950 http://scihub22266oqcxt.onion/10.3389/fimmu.2020.595950 33643285!7905033!33643285     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33643285&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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33643285.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Immunol 2020 ; 11 (ä): 595950 Nephropedia Template TP {{tp|p=33643285|t=2020. VISTA: A Target to Manage the Innate Cytokine Storm |pdf=|usr=}}{{33643285}} gab.com Text VISTA: A Target to Manage the Innate Cytokine Storm JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33643285 #FOAvip In recent years, the success of immunotherapy targeting immunoregulatory receptors (immune checkpoints) in cancer have generated enthusiastic support to target these receptors in a wide range of other immune related diseases. While the overwhelming focus has been on blockade of these inhibitory pathways to augment immunity, agonistic triggering via these receptors offers the promise of dampening pathogenic inflammatory responses. V-domain Ig suppressor of T cell activation (VISTA) has emerged as an immunoregulatory receptor with constitutive expression on both the T cell and myeloid compartments, and whose agonistic targeting has proven a unique avenue relative to other checkpoint pathways to suppress pathologies mediated by the innate arm of the immune system. VISTA agonistic targeting profoundly changes the phenotype of human monocytes towards an anti-inflammatory cell state, as highlighted by striking suppression of the canonical markers CD14 and Fcgammar3a (CD16), and the almost complete suppression of both the interferon I (IFN-I) and antigen presentation pathways. The insights from these very recent studies highlight the impact of VISTA agonistic targeting of myeloid cells, and its potential therapeutic implications in the settings of hyperinflammatory responses such as cytokine storms, driven by dysregulated immune responses to viral infections (with a focus on COVID-19) and autoimmune diseases. Collectively, these findings suggest that the VISTA pathway plays a conserved, non-redundant role in myeloid cell function. Twit Text FOAVip VISTA: A Target to Manage the Innate Cytokine Storm ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33643285 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33643285 #FOAvip English Wikipedia <ref>{{Cite pmid|33643285}}</ref> VISTA: A Target to Manage the Innate Cytokine Storm #MMPMID33643285 ElTanbouly MA; Zhao Y; Schaafsma E; Burns CM; Mabaera R; Cheng C; Noelle RJ Front Immunol 2020[]; 11 (ä): 595950 PMID33643285show ga In recent years, the success of immunotherapy targeting immunoregulatory receptors (immune checkpoints) in cancer have generated enthusiastic support to target these receptors in a wide range of other immune related diseases. While the overwhelming focus has been on blockade of these inhibitory pathways to augment immunity, agonistic triggering via these receptors offers the promise of dampening pathogenic inflammatory responses. V-domain Ig suppressor of T cell activation (VISTA) has emerged as an immunoregulatory receptor with constitutive expression on both the T cell and myeloid compartments, and whose agonistic targeting has proven a unique avenue relative to other checkpoint pathways to suppress pathologies mediated by the innate arm of the immune system. VISTA agonistic targeting profoundly changes the phenotype of human monocytes towards an anti-inflammatory cell state, as highlighted by striking suppression of the canonical markers CD14 and Fcgammar3a (CD16), and the almost complete suppression of both the interferon I (IFN-I) and antigen presentation pathways. The insights from these very recent studies highlight the impact of VISTA agonistic targeting of myeloid cells, and its potential therapeutic implications in the settings of hyperinflammatory responses such as cytokine storms, driven by dysregulated immune responses to viral infections (with a focus on COVID-19) and autoimmune diseases. Collectively, these findings suggest that the VISTA pathway plays a conserved, non-redundant role in myeloid cell function. |Animals[MESH] |Antigen Presentation/immunology[MESH] |B7 Antigens/*agonists/antagonists & inhibitors/immunology[MESH] |CD4-Positive T-Lymphocytes/immunology[MESH] |COVID-19/*pathology[MESH] |Cytokine Release Syndrome/immunology/pathology/*prevention & control[MESH] |GPI-Linked Proteins/antagonists & inhibitors[MESH] |Humans[MESH] |Immunotherapy[MESH] |Interferon Type I/antagonists & inhibitors[MESH] |Lipopolysaccharide Receptors/antagonists & inhibitors[MESH] |Lymphocyte Activation/immunology[MESH] |Mice[MESH] |Myeloid Cells/*immunology[MESH] |Receptors, IgG/antagonists & inhibitors[MESH]VISTA: A Target to Manage the Innate Cytokine Storm (epmc).pdf DeepDyve Pubget Overpricing