Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/12579
Title: Type I Interferon Suppresses Type II Interferon–Triggered Human Anti-Mycobacterial Responses
Authors: Teles, Rosane M. B.
Graeber, Thomas G.
Krutzik, Stephan R.
Montoya, Dennis
Schenk, Mirjam
Lee, Delphine J.
Komisopoulou, Evangelia
Kelly-Scumpia, Kindra
Chun, Rene
Iyer, Shankar S.
Sarno, Euzenir Nunes
Rea, Thomas H.
Hewison, Martin
Adams, John S.
Popper, Stephen J.
Relman, David A.
Stenger, Steffen
Bloom, Barry R.
Cheng, Genhong
Modlin, Robert L.
Affilliation: University of California. David Geffen School of Medicine. Division of Dermatology. Los Angeles, CA, USA.
University of California. Department of Molecular and Medical Pharmacology. California NanoSystems Institute. Johnson Comprehensive Cancer Center. Institute for Molecular Medicine. Crump Institute for Molecular Imaging. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. Division of Dermatology. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. Division of Dermatology. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. Division of Dermatology. Los Angeles, CA, USA.
John Wayne Cancer Institute. Department of Translational Immunology. Santa Monica, CA, USA.
University of California. Department of Molecular and Medical Pharmacology. California NanoSystems Institute. Johnson Comprehensive Cancer Center. Institute for Molecular Medicine. Crump Institute for Molecular Imaging. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. Division of Dermatology. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. UCLA/Orthopedic Hospital Department of Orthopedic Surgery. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. Department of Microbiology, Immunology and Molecular Genetics. Los Angeles, CA, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Ri de Janeiro, RJ, Brasil.
University of Southern California School of Medicine. Department of Dermathology. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. UCLA/Orthopedic Hospital Department of Orthopedic Surgery. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. UCLA/Orthopedic Hospital Department of Orthopedic Surgery. Los Angeles, CA, USA.
Stanford University School of Medicine. Department of Microbiology and Immunology. Department of Medicine. Stanford, CA, USA .
Stanford University School of Medicine. Department of Microbiology and Immunology. Department of Medicine. Stanford, CA, USA / 9Veterans Affairs Palo Alto Health Care System. Palo Alto, CA, USA.
University Hospital of Ulm. Institute for Medical Microbiology and Hygiene. Germany.
Harvard School of Public Health. Boston, MA, USA.
University of California. David Geffen School of Medicine. Department of Microbiology, Immunology and Molecular Genetics. Los Angeles, CA, USA.
University of California. David Geffen School of Medicine. Division of Dermatology. Los Angeles, CA, USA / University of California. David Geffen School of Medicine. Department of Microbiology, Immunology and Molecular Genetics. Los Angeles, CA, USA.
Abstract: Type I interferons (IFN-a and IFN-b) are important for protection against many viral infections, whereas type II interferon (IFN-g) is essential for host defense against some bacterial and parasitic pathogens. Study of IFN responses in human leprosy revealed an inverse correlation between IFN-b and IFN-g gene expression programs. IFN-g and its downstream vitamin D–dependent antimicrobial genes were preferentially expressed in self-healing tuberculoid lesions and mediated antimicrobial activity against the pathogen Mycobacterium leprae in vitro. In contrast, IFN-b and its downstream genes, including interleukin-10 (IL-10), were induced in monocytes by M. leprae in vitro and preferentially expressed in disseminated and progressive lepromatous lesions. The IFN-g–induced macrophage vitamin D–dependent antimicrobial peptide response was inhibited by IFN-b and by IL-10, suggesting that the differential production of IFNs contributes to protection versus pathogenesis in some human bacterial infections.
Keywords: Type I interferons (IFN-a and IFN-b)
type II interferon (IFN-g)
Leprosy
Anti-Mycobacterial
Mycobacterium leprae
DeCS: Mycobacterium leprae
Hanseniase
Interferon Tipo I
Interferon gama
Issue Date: 2013
Publisher: American Association for the Advancement of Science
Citation: TELES, Rosane M. B. et al. Type I Interferon Suppresses Type II Interferon–Triggered Human Anti-Mycobacterial Responses. Science, v.339, p.1448-1453, March 2013.
DOI: 10.1126/science.1233665
ISSN: 1095-9203
Copyright: open access
Appears in Collections:IOC - Artigos de Periódicos

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