Review
Cell Death and Differentiation (2009) 16, 57–69; doi:10.1038/cdd.2008.130; published online 5 September 2008
Eating the enemy within: autophagy in infectious diseases
Edited by G Kroemer
1Howard Hughes Medical Institute and Departments of Internal Medicine and Microbiology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA
Correspondence: B Levine, Department of Internal Medicine, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA. Tel: 214 648 0493; Fax: 214 648 0284; E-mail: beth.levine@utsouthwestern.edu
Received 3 July 2008; Revised 14 July 2008; Accepted 30 July 2008; Published online 5 September 2008.
Abstract
Autophagy is emerging as a central component of antimicrobial host defense against diverse viral, bacterial, and parasitic infections. In addition to pathogen degradation, autophagy has other functions during infection such as innate and adaptive immune activation. As an important host defense pathway, microbes have also evolved mechanisms to evade, subvert, or exploit autophagy. Additionally, some fungal pathogens harness autophagy within their own cells to promote pathogenesis. This review will highlight our current understanding of autophagy in infection, focusing on the most recent advances in the field, and will discuss the potential implications of these studies in the design of anti-infective therapeutics.
Keywords:
autophagy, immunity, infection
Abbreviations:
PRR, pattern recognition receptors; PAMPs, pathogen associated molecular patterns; TLRs, Toll-like receptors; BCG, M. tuberculosis var bovis; NLRs, Nod-like receptors; TTSS, Type-III secretion system; LLO, listeriolysin O; HSV-1, herpes simplex virus type 1; LC3, microtubule-associated protein 1 light chain 3
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