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 Immunoljournal_title
Clinical and experimental immunologyauthors
Ní Cheallaigh C,Keane J,Lavelle EC,Hope JC,Harris Jdoi
10.1111/j.1365-2249.2011.04381.xsubject
Has Abstractpub_date
2011-06-01 00:00:00pages
291-300issue
3eissn
0009-9104issn
1365-2249journal_volume
164pub_type
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