Autophagy in the immune response to tuberculosis: clinical perspectives

C. Ni Cheallaigh, J. Keane, E.C. Lavelle, J.C. Hope, J. Harris

Research output: Contribution to journalArticlepeer-review


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)-alpha and interferon (IFN)-gamma, 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.
Original languageUndefined/Unknown
Pages (from-to)291-300
Number of pages10
JournalClinical & Experimental Immunology
Issue number3
Publication statusPublished - 2011

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