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Respiratory Failure & Mechanical Ventilation

Public·894 members

This is a good review article of GBS, and I thought it would of interest to you to share. @Everyone


https://www.frontiersin.org/articles/10.3389/fphar.2021.608130/full


Pharmacological therapeutic targets of GBS. The hyperreactive cellular and/or humoral immune responses in GBS are the main targets of current pharmacological interventions. IVIg can inhibit the production of pathogenic antibodies and pro-inflammatory mediators released by T helper cells and activated B cells via functioning on Tregs. IVIg also promotes the dimerization of antiganglioside antibodies and inhibits APCs to alleviate immune responses. PE mainly replaces plasm rich in antiganglioside antibodies and pro-inflammatory mediators with fresh frozen plasma/albumin. Eculizumab, nafamostat mesilate, and rEV576 are complement inhibitors that can prevent MAC formation. IFN-β attenuates inflammation induced by cytokines and chemokines. Cysteine protease degrades pathogenic antibodies and mitigates hyperreactive immune responses. Abbreviations: APC, antigen-presenting cell; C. jejuni, Campylobacter jejuni; GBS, Guillain–Barré syndrome; IFN-β, interferon β; IL, interleukin; IVIg, intravenous immunoglobulin; LOS, lipo-oligosaccharide; MAC, membrane attack complex; PE, plasma exchange; TGF-β, transform growth factor β; Th cell, T helper cell; TLR, Toll-like receptor; TNF-α, tumor necrosis factor-α; Treg, regulatory T cell.


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