Autophagy in the immune response to tuberculosis: clinical perspectives.
Affiliation
Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin and St James's Hospital, Dublin 8, Ireland.Issue Date
2011-06MeSH
AnimalsAntigen Presentation
Antitubercular Agents
Autophagy
Cytokines
Humans
Immunity
Mycobacterium tuberculosis
Th1-Th2 Balance
Tuberculosis
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Autophagy in the immune response to tuberculosis: clinical perspectives. 2011, 164 (3):291-300 Clin. Exp. Immunol.Journal
Clinical and experimental immunologyDOI
10.1111/j.1365-2249.2011.04381.xPubMed ID
21438870Additional Links
http://www.ncbi.nlm.nih.gov/pubmed/21438870Abstract
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.Item Type
ArticleLanguage
enISSN
1365-2249ae974a485f413a2113503eed53cd6c53
10.1111/j.1365-2249.2011.04381.x
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