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10.1016/j.immuni.2021.04.002 http://scihub22266oqcxt.onion/10.1016/j.immuni.2021.04.002 33915108!8080416!33915108     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33915108&cmd=llinks): Failed to open stream: HTTP request failed! 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Notch4 signaling limits regulatory T-cell-mediated tissue repair and promotes severe lung inflammation in viral infections |pdf=|usr=}}{{33915108}} gab.com Text Notch4 signaling limits regulatory T-cell-mediated tissue repair and promotes severe lung inflammation in viral infections JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=33915108 #FOAvip A cardinal feature of COVID-19 is lung inflammation and respiratory failure. In a prospective multi-country cohort of COVID-19 patients, we found that increased Notch4 expression on circulating regulatory T (Treg) cells was associated with disease severity, predicted mortality, and declined upon recovery. Deletion of Notch4 in Treg cells or therapy with anti-Notch4 antibodies in conventional and humanized mice normalized the dysregulated innate immunity and rescued disease morbidity and mortality induced by a synthetic analog of viral RNA or by influenza H1N1 virus. Mechanistically, Notch4 suppressed the induction by interleukin-18 of amphiregulin, a cytokine necessary for tissue repair. Protection by Notch4 inhibition was recapitulated by therapy with Amphiregulin and, reciprocally, abrogated by its antagonism. Amphiregulin declined in COVID-19 subjects as a function of disease severity and Notch4 expression. Thus, Notch4 expression on Treg cells dynamically restrains amphiregulin-dependent tissue repair to promote severe lung inflammation, with therapeutic implications for COVID-19 and related infections. Twit Text FOAVip Notch4 signaling limits regulatory T-cell-mediated tissue repair and promotes severe lung inflammation in viral infections ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=33915108 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33915108 #FOAvip English Wikipedia <ref>{{Cite pmid|33915108}}</ref> Notch4 signaling limits regulatory T-cell-mediated tissue repair and promotes severe lung inflammation in viral infections #MMPMID33915108 Harb H; Benamar M; Lai PS; Contini P; Griffith JW; Crestani E; Schmitz-Abe K; Chen Q; Fong J; Marri L; Filaci G; Del Zotto G; Pishesha N; Kolifrath S; Broggi A; Ghosh S; Gelmez MY; Oktelik FB; Cetin EA; Kiykim A; Kose M; Wang Z; Cui Y; Yu XG; Li JZ; Berra L; Stephen-Victor E; Charbonnier LM; Zanoni I; Ploegh H; Deniz G; De Palma R; Chatila TA Immunity 2021[Jun]; 54 (6): 1186-1199.e7 PMID33915108show ga A cardinal feature of COVID-19 is lung inflammation and respiratory failure. In a prospective multi-country cohort of COVID-19 patients, we found that increased Notch4 expression on circulating regulatory T (Treg) cells was associated with disease severity, predicted mortality, and declined upon recovery. Deletion of Notch4 in Treg cells or therapy with anti-Notch4 antibodies in conventional and humanized mice normalized the dysregulated innate immunity and rescued disease morbidity and mortality induced by a synthetic analog of viral RNA or by influenza H1N1 virus. Mechanistically, Notch4 suppressed the induction by interleukin-18 of amphiregulin, a cytokine necessary for tissue repair. Protection by Notch4 inhibition was recapitulated by therapy with Amphiregulin and, reciprocally, abrogated by its antagonism. Amphiregulin declined in COVID-19 subjects as a function of disease severity and Notch4 expression. Thus, Notch4 expression on Treg cells dynamically restrains amphiregulin-dependent tissue repair to promote severe lung inflammation, with therapeutic implications for COVID-19 and related infections. |*Host-Pathogen Interactions/immunology[MESH] |*Immunity, Cellular[MESH] |*Signal Transduction[MESH] |Amphiregulin/pharmacology[MESH] |Animals[MESH] |Biomarkers[MESH] |Cytokines/metabolism[MESH] |Disease Models, Animal[MESH] |Disease Susceptibility[MESH] |Humans[MESH] |Immunohistochemistry[MESH] |Immunomodulation/drug effects[MESH] |Inflammation Mediators/metabolism[MESH] |Influenza A virus/physiology[MESH] |Lung/immunology/metabolism/pathology/virology[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |Pneumonia, Viral/*etiology/*metabolism/pathology[MESH] |Receptor, Notch4/antagonists & inhibitors/genetics/*metabolism[MESH] |Severity of Illness Index[MESH]Notch4 signaling limits regulatory T-cell-mediated tissue repair and p(epmc).pdf DeepDyve Pubget Overpricing