Type I Interferon Suppresses Type II Interferon–Triggered Human Anti-Mycobacterial Responses
Autor: | Steffen Stenger, Robert L. Modlin, Dennis Montoya, Martin Hewison, Genhong Cheng, Rosane M. B. Teles, Shankar S. Iyer, Stephen J. Popper, Mirjam Schenk, Thomas H. Rea, Evangelia Komisopoulou, Kindra M. Kelly-Scumpia, David A. Relman, Thomas G. Graeber, Euzenir Nunes Sarno, Rene F. Chun, John S. Adams, Barry R. Bloom, Delphine J. Lee, Stephan R. Krutzik |
---|---|
Rok vydání: | 2013 |
Předmět: |
beta-Defensins
Monocytes Article Microbiology Interferon-gamma Cathelicidins Interferon medicine Humans Tuberculosis Macrophage Interferon gamma RNA Messenger Pathogen Mycobacterium leprae 25-Hydroxyvitamin D3 1-alpha-Hydroxylase Microbial Viability Multidisciplinary biology Interferon-beta Antimicrobial biology.organism_classification Leprosy Tuberculoid Virology Interleukin-10 Up-Regulation Leprosy Lepromatous Interleukin 10 Beta defensin Receptors Calcitriol Transcriptome Antimicrobial Cationic Peptides medicine.drug |
Zdroj: | Science. 339:1448-1453 |
ISSN: | 1095-9203 0036-8075 |
Popis: | Type I interferons (IFN-α and IFN-β) are important for protection against many viral infections, whereas type II interferon (IFN-γ) is essential for host defense against some bacterial and parasitic pathogens. Study of IFN responses in human leprosy revealed an inverse correlation between IFN-β and IFN-γ gene expression programs. IFN-γ 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-β 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-γ-induced macrophage vitamin D-dependent antimicrobial peptide response was inhibited by IFN-β and by IL-10, suggesting that the differential production of IFNs contributes to protection versus pathogenesis in some human bacterial infections. |
Databáze: | OpenAIRE |
Externí odkaz: |