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Toxicology. 2017 Nov 1;391:54-63. doi: 10.1016/j.tox.2017.07.016. Epub 2017 Jul 29.

Mitochondrial dysfunction as a trigger of innate immune responses and inflammation.

Author information

1
Department of Microbial Pathogenesis and Immunology, Texas A&M University Health Science Center, 470 Reynolds Medical Building, TAMU 1114, College Station, TX 77843, USA. Electronic address: awest@tamhsc.edu.

Abstract

A growing literature indicates that mitochondria are key participants in innate immune pathways, functioning as both signaling platforms and contributing to effector responses. In addition to regulating antiviral signaling and antibacterial immunity, mitochondria are also important drivers of inflammation caused by sterile injury. Much research on mitochondrial control of immunity now centers on understanding how mitochondrial constituents released during cellular damage simulate the innate immune system. When mitochondrial integrity is compromised, mitochondrial damage-associated molecular patterns engage pattern recognition receptors, trigger inflammation, and promote pathology in an expanding list of diseases. Here, I review the emerging knowledge of mitochondrial dysfunction in innate immune responses and discuss how environmental exposures may induce mitochondrial damage to potentiate inflammation and human disease.

PMID:
28765055
DOI:
10.1016/j.tox.2017.07.016
[Indexed for MEDLINE]

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