Mitochondria in innate immunity

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Presentation transcript:

Mitochondria in innate immunity Release of mitochondrial DAMPs triggers cell death and inflammatory pathways. (A) Severe trauma can induce the release of mitochondrial DNA (mtDNA), which is detected by TLR9 located on the neutrophil surface, and thus activates p38 MAP kinase. N‐formyl peptides are released by mitochondria and recruit polymorphonuclear neutrophils (PMNs) by binding to the formyl‐peptide receptor 1 (FPR1) expressed on their surface. (B) Autophagy‐deficient cells accumulate defective mitochondria, which release mtDNA into the cytosol, triggering activation of the inflammasome through an undefined cytosolic sensor. (C) Cell death signals induce the release of cytochrome c into the cytosol, leading to the recruitment of APAF1 and pro‐caspase 9 into a multiprotein complex known as the apoptosome. After activation, caspase 9 induces apoptosis by cleaving effector caspases. DAMP, danger‐associated molecular pattern; IL, interleukin; MAPK, mitogen‐activated protein kinase; TLR, Toll‐like receptor. IF THIS IMAGE HAS BEEN PROVIDED BY OR IS OWNED BY A THIRD PARTY, AS INDICATED IN THE CAPTION LINE, THEN FURTHER PERMISSION MAY BE NEEDED BEFORE ANY FURTHER USE. PLEASE CONTACT WILEY'S PERMISSIONS DEPARTMENT ON PERMISSIONS@WILEY.COM OR USE THE RIGHTSLINK SERVICE BY CLICKING ON THE 'REQUEST PERMISSIONS' LINK ACCOMPANYING THIS ARTICLE. WILEY OR AUTHOR OWNED IMAGES MAY BE USED FOR NON-COMMERCIAL PURPOSES, SUBJECT TO PROPER CITATION OF THE ARTICLE, AUTHOR, AND PUBLISHER. EMBO Rep, Volume: 12, Issue: 9, Pages: 901-910, First published: 29 July 2011, DOI: (10.1038/embor.2011.157)