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

Nicholas, Sally A., Oniku, Abraham E., Sumbayev, Vadim V. (2010) Myeloid cell death associated with Toll-like receptor 7/8-mediated inflammatory response. Implication of ASK1, HIF-1alpha, IL-1beta and TNF-alpha. Molecular Immunology, 48 (1-3). pp. 240-247. ISSN 0161-5890. (doi:10.1016/j.molimm.2010.08.004) (Access to this publication is currently restricted. You may be able to access a copy if URLs are provided)

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http://dx.doi.org/10.1016/j.molimm.2010.08.004

Abstract

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-? and IL-1?. We have found that released IL-1? and TNF-? are involved in apoptosis of myeloid cells associated with TLR7/8-mediated inflammatory stress. The pro-apoptotic effect of released TNF-? in this case is much lower compared to that of IL-1?.

Item Type: Article
DOI/Identification number: 10.1016/j.molimm.2010.08.004
Uncontrolled keywords: Toll-like receptors; Inflammation; Apoptosis; IL-1beta; ASK1; TNF-alpha
Subjects: Q Science > QP Physiology (Living systems) > QP517 Biochemistry
Divisions: Faculties > Sciences > Medway School of Pharmacy
Depositing User: Vadim Sumbayev
Date Deposited: 08 Dec 2014 17:38 UTC
Last Modified: 29 May 2019 13:50 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/45796 (The current URI for this page, for reference purposes)
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