IL17A augments autophagy in Mycobacterium tuberculosis-infected monocytes from patients with active tuberculosis in association with the severity of the disease

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During mycobacterial infection, macroautophagy/autophagy, a process modulated by cytokines, is essential for mounting successful host responses. Autophagy collaborates with human immune responses against Mycobacterium tuberculosis (Mt) in association with specific IFNG secreted against the pathogen....

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Autor principal: Tateosian, N.L
Otros Autores: Pellegrini, J.M, Amiano, N.O, Rolandelli, A., Casco, N., Palmero, D.J, Colombo, M.I, García, V.E
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: Taylor and Francis Inc. 2017
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Biblioteca Central Dr. Luis F. Leloir (FCEN) de Universidad de Buenos Aires
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024 7 |2 scopus  |a 2-s2.0-85020641186 
024 7 |2 cas  |a gamma interferon, 82115-62-6; mitogen activated protein kinase 1, 137632-08-7; mitogen activated protein kinase 3, 137632-07-6; phosphatidylinositol 3 kinase, 115926-52-8; IFNG protein, human; IL17A protein, human; Interferon-gamma; Interleukin-17 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
100 1 |a Tateosian, N.L. 
245 1 0 |a IL17A augments autophagy in Mycobacterium tuberculosis-infected monocytes from patients with active tuberculosis in association with the severity of the disease 
260 |b Taylor and Francis Inc.  |c 2017 
270 1 0 |m García, V.E.; Departamento de Química Biológica. Facultad de Ciencias Exactas y Naturales. UBA, Ciudad Universitaria, Intendente G€iraldes 2160, Pabellón II, 4˚piso, Ciudad Universitaria (C1428EGA), Argentina; email: vgarcia@qb.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a During mycobacterial infection, macroautophagy/autophagy, a process modulated by cytokines, is essential for mounting successful host responses. Autophagy collaborates with human immune responses against Mycobacterium tuberculosis (Mt) in association with specific IFNG secreted against the pathogen. However, IFNG alone is not sufficient to the complete bacterial eradication, and other cytokines might be required. Actually, induction of Th1 and Th17 immune responses are required for protection against Mt. Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. Patients with active disease were classified as high responder (HR) or low responder (LR) according to their T cell responses against Mt. IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. Therefore, in severe tuberculosis patients' monocytes, IL17A was unable to augment autophagy because of a defect in the MAPK1/3 signaling pathway. In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. Our findings might contribute to recognize new targets for the development of novel therapeutic tools to fight the pathogen. © 2017 Taylor & Francis.  |l eng 
593 |a Departamento de Química Biológica. Facultad de Ciencias Exactas y Naturales. UBA, Ciudad Universitaria, Buenos Aires, Argentina 
593 |a Universidad de Buenos Aires. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales (IQUIBICEN). Facultad de Ciencias Exactas y Naturales, Ciudad Universitaria, Buenos Aires, Argentina 
593 |a División Tisioneumonología Hospital F.J. Muñiz, Buenos Aires, Argentina 
593 |a Instituto de Histología y Embriología de Mendoza, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo-CONICET, Mendoza, Argentina 
690 1 0 |a AUTOPHAGY 
690 1 0 |a CYTOKINES 
690 1 0 |a IFNG 
690 1 0 |a IL17A 
690 1 0 |a IMMUNE RESPONSE 
690 1 0 |a MYCOBACTERIUM TUBERCULOSIS 
690 1 0 |a PATIENTS 
690 1 0 |a BCG VACCINE 
690 1 0 |a CD14 ANTIGEN 
690 1 0 |a GAMMA INTERFERON 
690 1 0 |a INTERLEUKIN 17 
690 1 0 |a INTERLEUKIN 17 RECEPTOR 
690 1 0 |a INTERLEUKIN 17 RECEPTOR A 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 1 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 14 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 3 
690 1 0 |a PHOSPHATIDYLINOSITOL 3 KINASE 
690 1 0 |a TUBERCULOSTATIC AGENT 
690 1 0 |a UNCLASSIFIED DRUG 
690 1 0 |a GAMMA INTERFERON 
690 1 0 |a IFNG PROTEIN, HUMAN 
690 1 0 |a IL17A PROTEIN, HUMAN 
690 1 0 |a INTERLEUKIN 17 
690 1 0 |a ADHERENT CELL 
690 1 0 |a ARTICLE 
690 1 0 |a AUTOPHAGOSOME 
690 1 0 |a AUTOPHAGY 
690 1 0 |a BACTERIAL GENOME 
690 1 0 |a BACTERIAL GROWTH 
690 1 0 |a BACTERICIDAL ACTIVITY 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DISEASE CLASSIFICATION 
690 1 0 |a DISEASE SEVERITY 
690 1 0 |a ENZYME ACTIVATION 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a INTRACELLULAR SIGNALING 
690 1 0 |a LUNG TUBERCULOSIS 
690 1 0 |a LYSOSOME 
690 1 0 |a MONOCYTE 
690 1 0 |a MYCOBACTERIUM TUBERCULOSIS 
690 1 0 |a PERIPHERAL BLOOD MONONUCLEAR CELL 
690 1 0 |a PHAGOSOME 
690 1 0 |a PROTEIN PHOSPHORYLATION 
690 1 0 |a UPREGULATION 
690 1 0 |a CELL CULTURE 
690 1 0 |a IMMUNOLOGY 
690 1 0 |a MICROBIOLOGY 
690 1 0 |a MONOCYTE 
690 1 0 |a MYCOBACTERIUM TUBERCULOSIS 
690 1 0 |a PHYSIOLOGY 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a AUTOPHAGY 
690 1 0 |a CELLS, CULTURED 
690 1 0 |a HUMANS 
690 1 0 |a INTERFERON-GAMMA 
690 1 0 |a INTERLEUKIN-17 
690 1 0 |a MONOCYTES 
690 1 0 |a MYCOBACTERIUM TUBERCULOSIS 
690 1 0 |a SIGNAL TRANSDUCTION 
650 1 7 |2 spines  |a TUBERCULOSIS 
650 1 7 |2 spines  |a TUBERCULOSIS 
650 1 7 |2 spines  |a TUBERCULOSIS 
700 1 |a Pellegrini, J.M. 
700 1 |a Amiano, N.O. 
700 1 |a Rolandelli, A. 
700 1 |a Casco, N. 
700 1 |a Palmero, D.J. 
700 1 |a Colombo, M.I. 
700 1 |a García, V.E. 
773 0 |d Taylor and Francis Inc., 2017  |g v. 13  |h pp. 1191-1204  |k n. 7  |p Autophagy  |x 15548627  |t Autophagy 
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856 4 0 |u https://doi.org/10.1080/15548627.2017.1320636  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_15548627_v13_n7_p1191_Tateosian  |y Handle 
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