Myeloid cell death associated with Toll-like receptor 7/8-mediated inflammatory response Implication of ASK1, HIF-1alpha, IL-1beta and TNF-alpha

被引：10

作者：

Nicholas, Sally A. ^{[1
]}

Oniku, Abraham E. ^{[1
]}

Sumbayev, Vadim V. ^{[1
]}

机构：

[1] Univ Kent, Medway Sch Pharm, Chatham ME4 4TB, Kent, England

来源：

MOLECULAR IMMUNOLOGY | 2010年 / 48卷 / 1-3期

关键词：

Toll-like receptors; Inflammation; Apoptosis; IL; 1beta; ASK1; TNF alpha; HIF-1-ALPHA PROTEIN; INNATE IMMUNITY; APOPTOSIS; ACTIVATION; IL-1-BETA; PATHWAY;

D O I：

10.1016/j.molimm.2010.08.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Programmed cell death or apoptosis is an important part of the host innate immune defence especially against ssRNA viruses (influenza virus HIV-1 ebola virus hepatitis C virus and many others) Viral ssRNA is recognised by endosomal Toll-like receptors 7 and 8 (TLR7/8) which induce further stages of immune defence against these pathogens Some of the immune cells die because of inflammatory stress allowing for the selection of those cells which are resistant to stress-induced apoptosis and which are used in further stages of the host immune response On the other hand apoptosis could be used as an instrument to suppress the function of activated Inflammatory cells However the mechanisms underlying death of the inflammatory cells associated with stress Induced by ligands of TLR7/8 remain unclear In this study we have found that programmed death of human myeloid cells from different cell lines associated with ligand-induced TLR7/8-mediated inflammatory stress depends on activation of apoptosis signal-regulating kinase 1 (ASK1) This enzyme is however not required for the production of pro-inflammatory cytokines - TNF-alpha and IL-1 beta We have found that released IL-1 beta and TNF-alpha are involved in apoptosis of myeloid cells associated with TLR7/8-mediated inflammatory stress The pro-apoptotic effect of released TNF-alpha in this case is much lower compared to that of IL-1 beta (C) 2010 Elsevier Ltd All rights reserved

引用

页码：240 / 247

页数：8

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