Autophagy in the immune response to tuberculosis: clinical perspectives.

Hdl Handle:
http://hdl.handle.net/10147/136389
Title:
Autophagy in the immune response to tuberculosis: clinical perspectives.
Authors:
Ní Cheallaigh, C; Keane, J; Lavelle, E C; Hope, J C; Harris, J
Affiliation:
Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin and St James's Hospital, Dublin 8, Ireland.
Citation:
Autophagy in the immune response to tuberculosis: clinical perspectives. 2011, 164 (3):291-300 Clin. Exp. Immunol.
Journal:
Clinical and experimental immunology
Issue Date:
Jun-2011
URI:
http://hdl.handle.net/10147/136389
DOI:
10.1111/j.1365-2249.2011.04381.x
PubMed ID:
21438870
Additional Links:
http://www.ncbi.nlm.nih.gov/pubmed/21438870
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.
Item Type:
Article
Language:
en
MeSH:
Animals; Antigen Presentation; Antitubercular Agents; Autophagy; Cytokines; Humans; Immunity; Mycobacterium tuberculosis; Th1-Th2 Balance; Tuberculosis
ISSN:
1365-2249

Full metadata record

DC FieldValue Language
dc.contributor.authorNí Cheallaigh, Cen
dc.contributor.authorKeane, Jen
dc.contributor.authorLavelle, E Cen
dc.contributor.authorHope, J Cen
dc.contributor.authorHarris, Jen
dc.date.accessioned2011-07-20T08:34:25Z-
dc.date.available2011-07-20T08:34:25Z-
dc.date.issued2011-06-
dc.identifier.citationAutophagy in the immune response to tuberculosis: clinical perspectives. 2011, 164 (3):291-300 Clin. Exp. Immunol.en
dc.identifier.issn1365-2249-
dc.identifier.pmid21438870-
dc.identifier.doi10.1111/j.1365-2249.2011.04381.x-
dc.identifier.urihttp://hdl.handle.net/10147/136389-
dc.description.abstractA 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.-
dc.language.isoenen
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/21438870en
dc.subject.meshAnimals-
dc.subject.meshAntigen Presentation-
dc.subject.meshAntitubercular Agents-
dc.subject.meshAutophagy-
dc.subject.meshCytokines-
dc.subject.meshHumans-
dc.subject.meshImmunity-
dc.subject.meshMycobacterium tuberculosis-
dc.subject.meshTh1-Th2 Balance-
dc.subject.meshTuberculosis-
dc.titleAutophagy in the immune response to tuberculosis: clinical perspectives.en
dc.typeArticleen
dc.contributor.departmentDepartment of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin and St James's Hospital, Dublin 8, Ireland.en
dc.identifier.journalClinical and experimental immunologyen
dc.description.provinceLeinster-

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