Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1084/jem.20220236 http://scihub22266oqcxt.onion/10.1084/jem.20220236 35604387!9130030!35604387     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Exp+Med 2022 ; 219 (7): ä Nephropedia Template TP {{tp|p=35604387|t=2022. Realigning the LIGHT signaling network to control dysregulated inflammation |pdf=|usr=}}{{35604387}} gab.com Text Realigning the LIGHT signaling network to control dysregulated inflammation JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=35604387 #FOAvip Advances in understanding the physiologic functions of the tumor necrosis factor superfamily (TNFSF) of ligands, receptors, and signaling networks are providing deeper insight into pathogenesis of infectious and autoimmune diseases and cancer. LIGHT (TNFSF14) has emerged as an important modulator of critical innate and adaptive immune responses. LIGHT and its signaling receptors, herpesvirus entry mediator (TNFRSF14), and lymphotoxin beta receptor, form an immune regulatory network with two co-receptors of herpesvirus entry mediator, checkpoint inhibitor B and T lymphocyte attenuator, and CD160. Deciphering the fundamental features of this network reveals new understanding to guide therapeutic development. Accumulating evidence from infectious diseases points to the dysregulation of the LIGHT network as a disease-driving mechanism in autoimmune and inflammatory reactions in barrier organs, including coronavirus disease 2019 pneumonia and inflammatory bowel diseases. Recent clinical results warrant further investigation of the LIGHT regulatory network and application of target-modifying therapeutics for disease intervention. Twit Text FOAVip Realigning the LIGHT signaling network to control dysregulated inflammation ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=35604387 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35604387 #FOAvip English Wikipedia <ref>{{Cite pmid|35604387}}</ref> Realigning the LIGHT signaling network to control dysregulated inflammation #MMPMID35604387 Ware CF; Croft M; Neil GA J Exp Med 2022[Jul]; 219 (7): ä PMID35604387show ga Advances in understanding the physiologic functions of the tumor necrosis factor superfamily (TNFSF) of ligands, receptors, and signaling networks are providing deeper insight into pathogenesis of infectious and autoimmune diseases and cancer. LIGHT (TNFSF14) has emerged as an important modulator of critical innate and adaptive immune responses. LIGHT and its signaling receptors, herpesvirus entry mediator (TNFRSF14), and lymphotoxin beta receptor, form an immune regulatory network with two co-receptors of herpesvirus entry mediator, checkpoint inhibitor B and T lymphocyte attenuator, and CD160. Deciphering the fundamental features of this network reveals new understanding to guide therapeutic development. Accumulating evidence from infectious diseases points to the dysregulation of the LIGHT network as a disease-driving mechanism in autoimmune and inflammatory reactions in barrier organs, including coronavirus disease 2019 pneumonia and inflammatory bowel diseases. Recent clinical results warrant further investigation of the LIGHT regulatory network and application of target-modifying therapeutics for disease intervention. |*COVID-19[MESH] |*Receptors, Tumor Necrosis Factor, Member 14[MESH] |Humans[MESH] |Inflammation[MESH] |Signal Transduction[MESH]Realigning the LIGHT signaling network to control dysregulated inflamm(epmc).pdf DeepDyve Pubget Overpricing