id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-003013-h8txbd3p	Kim, Sena	Differential Regulation of Toll-Like Receptor-Mediated Cytokine Production by Unfolded Protein Response	2018-04-24		.txt	text/plain	3706	205	35	Under ER stress, unfolded protein response (UPR) signaling pathways participate in upregulating inflammatory cytokine production via NF-kappaB, MAPK, and GSK-3β. Toll-like receptor (TLRs) can recognize pathogenassociated molecular patterns (PAMPs) and dangerassociated molecular patterns (DAMPs) and induce TLRmediated intracellular signaling cascades to eliminate the pathogens through the production of proinflammatory cytokines including TNF-α, IL-6, IL-1β, and IL-8, but its uncontrolled activation can damage the host [9] . ER stress has been shown to regulate proinflammatory cytokine production, which are mediated by TLR signaling cascade components such as NF-kappaB, MAPK, and GSK-3β. In addition, ER stress shares TLR-mediated signaling components with pro-and anti-inflammatory cytokine productions, leading to the activation of NF-kappaB and MAPKs. The XBP1 deletion or chemical chaperone treatment in macrophages alleviates proinflammatory cytokine production by LPS. Toll-like receptor-mediated activation of intracellular signaling pathways results in increased production of proinflammatory cytokines including TNF-α, IL-6, and IL-1β. Endoplasmic reticulum stress-induced IRE1α activation mediates cross-talk of GSK-3β and XBP-1 to regulate inflammatory cytokine production	./cache/cord-003013-h8txbd3p.txt	./txt/cord-003013-h8txbd3p.txt