Autophagy in the immune response to tuberculosis: clinical perspectives.

Abstract

A growing body of evidence points to autophagy as an essential component in the immune response to tuberculosis. Autophagy is a direct mechanism of killing intracellular Mycobacterium tuberculosis and also acts as a modulator of proinflammatory cytokine secretion. In addition, autophagy plays a key role in antigen processing and presentation. Autophagy is modulated by cytokines; it is stimulated by T helper type 1 (Th1) cytokines such as tumour necrosis factor (TNF)-α and interferon (IFN)-γ, and is inhibited by the Th2 cytokines interleukin (IL)-4 and IL-13 and the anti-inflammatory cytokine IL-10. Vitamin D, via cathelicidin, can also induce autophagy, as can Toll-like receptor (TLR)-mediated signals. Autophagy-promoting agents, administered either locally to the lungs or systemically, could have a clinical application as adjunctive treatment of drug-resistant and drug-sensitive tuberculosis. Moreover, vaccines which effectively induce autophagy could be more successful in preventing acquisition or reactivation of latent tuberculosis.

• Authors: C Ní Cheallaigh, J Keane, E C Lavelle, J C Hope, J Harris
• Journal: Clinical and experimental immunology (Clin Exp Immunol) Vol. 164 Issue 3 Pg. 291-300 (Jun 2011) ISSN: 1365-2249 [Electronic] England
• PMID: 21438870 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: © 2011 The Authors. Clinical and Experimental Immunology © 2011 British Society for Immunology.

Chemical References

• Antitubercular Agents
• Cytokines

Topics

• Animals
• Antigen Presentation (drug effects)
• Antitubercular Agents (therapeutic use)
• Autophagy (drug effects, immunology)
• Cytokines (immunology)
• Humans
• Immunity
• Mycobacterium tuberculosis (immunology)
• Th1-Th2 Balance (drug effects)
• Tuberculosis (immunology, therapy)