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 N; Rea, Thomas H; Hewison, Martin; Adams, John S; Popper, Stephen J; Relman, David A; Stenger, Steffen; Bloom, Barry R; Cheng, Genhong and Modlin, Robert L (2013). Type I interferon suppresses type II interferon-triggered human anti-mycobacterial responses. Science, 339(6126), pp. 1448-1453. American Association for the Advancement of Science 10.1126/science.1233665
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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.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Service Sector > Institute of Pathology > Immunopathology |
UniBE Contributor: |
Schenk, Mirjam |
ISSN: |
0036-8075 |
Publisher: |
American Association for the Advancement of Science |
Language: |
English |
Submitter: |
Mirjam Schenk |
Date Deposited: |
25 Jul 2017 15:39 |
Last Modified: |
05 Dec 2022 15:06 |
Publisher DOI: |
10.1126/science.1233665 |
PubMed ID: |
23449998 |
BORIS DOI: |
10.7892/boris.102299 |
URI: |
https://boris.unibe.ch/id/eprint/102299 |
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