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- W2099731256 abstract "Summary 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." @default.
- W2099731256 created "2016-06-24" @default.
- W2099731256 creator A5016868088 @default.
- W2099731256 creator A5078961892 @default.
- W2099731256 creator A5082654662 @default.
- W2099731256 creator A5088266692 @default.
- W2099731256 creator A5090537154 @default.
- W2099731256 date "2011-03-25" @default.
- W2099731256 modified "2023-10-16" @default.
- W2099731256 title "Autophagy in the immune response to tuberculosis: clinical perspectives" @default.
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