Pathogens and Dead Cells Cooperate with Cytokines in Activating the Innate and Adaptive Response

European Journal of Inflammation

Editorial

J.E. Belizário¹ 

[1] Dr José E. Belizário, Department of Pharmacology, ICB, USP, Avenida Lineu Prestes, 1524-CEP05508-900, São Paulo, SP, Brazil, Fax: ++55 1130917218, e-mail: ;

关键词: cytokines;    inflammation;    innate and adaptive response;    TLR;    NLR;    apoptosis;    necrosis;    autophagy and pyroptosis;   

DOI  :  10.1177/1721727X1100900101

 received in 2010-03-30, accepted in 2011-01-07,  发布年份 2011

来源: Sage Journals

【 摘 要 】

After microbial invasion and tissue damage, a set of cytokines, including interleukin-1α (IL-1α), IL-1β, IL-6, IL-18 and tumor necrosis factor-α (TNF-α), and microbial and endogenous molecules named pathogen-associated molecular pattern (PAMPs) and damage-associated molecular pattern (DAMPs), are released from activated leukocytes and dead cells and bind to immune receptors to induce the innate and adaptive response. The intracellular signals induced by the multiprotein complex formed by the Toll-like receptors/IL-1 receptors (TLRs), NOD-like receptors (NLRs) and tumor necrosis factor-α receptors (TNFRs) and their ligands and downstream effectors lead to the activation of NF-κB (NFkappaB) and the interferon regulatory factor (IRF) transcription factors and thereby the synthesis of pro- and anti-inflammatory genes as well as pro- and anti-cell death genes. Depending on cell-intrinsic and extrinsic biochemical events elicited by an inflammatory response, the cells die via apoptosis, necrosis, pyroptosis or autophagy cell death program. This article resumes our current understanding of these processes and how they influence inflammation.

【 授权许可】

Unknown   
© 2011 SAGE Publications