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.

journal_name

Clin Exp Immunol

authors

Ní Cheallaigh C,Keane J,Lavelle EC,Hope JC,Harris J

doi

10.1111/j.1365-2249.2011.04381.x

subject

Has Abstract

pub_date

2011-06-01 00:00:00

pages

291-300

issue

3

eissn

0009-9104

issn

1365-2249

journal_volume

164

pub_type

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