title: 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: Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin and St James's Hospital, Dublin 8, Ireland.
authors: C
authors: C
authors: Ní Cheallaigh
authors: J
authors: J
authors: Keane
authors: E C
authors: EC
authors: Lavelle
authors: J C
authors: JC
authors: Hope
authors: J
authors: J
authors: Harris
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000187:drug effects; D000995:Antitubercular Agents / Q000627:therapeutic use; D001343:Autophagy / Q000187:drug effects / Q000276:immunology; D016207:Cytokines / Q000276:immunology*; D006801:Humans; D007109:Immunity; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D058408:Th1-Th2 Balance / Q000187:drug effects; D014376:Tuberculosis / Q000276:immunology* / Q000628:therapy
chemical_list: D000995:Antitubercular Agents; D016207:Cytokines