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Curr Opin Microbiol. 2013 Jun;16(3):355-65. doi: 10.1016/j.mib.2013.05.003. Epub 2013 Jun 18.

Autophagy as an immune effector against tuberculosis.

Author information

1
Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.

Abstract

The now well-accepted innate immunity paradigm that autophagy acts as a cell-autonomous defense against intracellular bacteria has its key origins in studies with Mycobacterium tuberculosis, an important human pathogen and a model microorganism infecting macrophages. A number of different factors have been identified that play into the anti-mycobacterial functions of autophagy, and recent in vivo studies in the mouse model of tuberculosis have uncovered additional anti-inflammatory and tissue-sparing functions of autophagy. Complementing these observations, genome wide association studies indicate a considerable overlap between autophagy, human susceptibility to mycobacterial infections and predisposition loci for inflammatory bowel disease. Finally, recent studies show that autophagy is an important regulator and effector of IL-1 responses, and that autophagy intersects with type I interferon pathology-modulating responses.

PMID:
23790398
PMCID:
PMC3742717
DOI:
10.1016/j.mib.2013.05.003
[Indexed for MEDLINE]
Free PMC Article

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