IL-26 contributes to host defense against intracellular bacteria.

Détails

ID Serval
serval:BIB_009CF10E644A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
IL-26 contributes to host defense against intracellular bacteria.
Périodique
The Journal of clinical investigation
Auteur(s)
Dang A.T., Teles R.M., Weiss D.I., Parvatiyar K., Sarno E.N., Ochoa M.T., Cheng G., Gilliet M., Bloom B.R., Modlin R.L.
ISSN
1558-8238 (Electronic)
ISSN-L
0021-9738
Statut éditorial
Publié
Date de publication
02/04/2019
Peer-reviewed
Oui
Volume
129
Numéro
5
Pages
1926-1939
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Résumé
IL-26 is an antimicrobial protein secreted by Th17 cells that has the ability to directly kill extracellular bacteria. To ascertain whether IL-26 contributes to host defense against intracellular bacteria, we studied leprosy, caused by the obligate intracellular pathogen Mycobacterium leprae, as a model. Analysis of leprosy skin lesions by gene expression profiling and immunohistology revealed that IL-26 was more strongly expressed in lesions from the self-limited tuberculoid compared with expression in progressive lepromatous patients. IL-26 directly bound to M. leprae in axenic culture and reduced bacteria viability. Furthermore, IL-26, when added to human monocyte-derived macrophages infected with M. leprae, entered the infected cell, colocalized with the bacterium, and reduced bacteria viability. In addition, IL-26 induced autophagy via the cytoplasmic DNA receptor stimulator of IFN genes (STING), as well as fusion of phagosomes containing bacilli with lysosomal compartments. Altogether, our data suggest that the Th17 cytokine IL-26 contributes to host defense against intracellular bacteria.
Mots-clé
Autophagy, Cytokines/immunology, Gene Expression Profiling, Humans, Interleukins/immunology, Leprosy, Lepromatous/microbiology, Leprosy, Tuberculoid/microbiology, Lysosomes/immunology, Lysosomes/microbiology, Macrophages/immunology, Monocytes/cytology, Mycobacterium leprae, Mycobacterium tuberculosis, Phagosomes/immunology, Recombinant Proteins/immunology, Signal Transduction, Th17 Cells/immunology, Cellular immune response, Immunology, Infectious disease
Pubmed
Web of science
Open Access
Oui
Création de la notice
15/04/2019 9:31
Dernière modification de la notice
27/04/2020 6:20
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