Publikationsdatum:
2013-03-02
Beschreibung:
Type I interferons (IFN-alpha and IFN-beta) are important for protection against many viral infections, whereas type II interferon (IFN-gamma) is essential for host defense against some bacterial and parasitic pathogens. Study of IFN responses in human leprosy revealed an inverse correlation between IFN-beta and IFN-gamma gene expression programs. IFN-gamma 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-beta 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-gamma-induced macrophage vitamin D-dependent antimicrobial peptide response was inhibited by IFN-beta and by IL-10, suggesting that the differential production of IFNs contributes to protection versus pathogenesis in some human bacterial infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653587/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653587/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉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 -- Modlin, Robert L -- P50 AR063020/AR/NIAMS NIH HHS/ -- R01 AI022553/AI/NIAID NIH HHS/ -- R01 AI047868/AI/NIAID NIH HHS/ -- R01 AI056154/AI/NIAID NIH HHS/ -- R01 AI082575/AI/NIAID NIH HHS/ -- R01 AR040312/AR/NIAMS NIH HHS/ -- R01 AR059126/AR/NIAMS NIH HHS/ -- T32 CA009120/CA/NCI NIH HHS/ -- UL1TR000124/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1448-53. doi: 10.1126/science.1233665. Epub 2013 Feb 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449998" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
25-Hydroxyvitamin D3 1-alpha-Hydroxylase/genetics/metabolism
;
Antimicrobial Cationic Peptides/genetics/metabolism
;
Humans
;
Interferon-beta/genetics/*immunology/metabolism
;
Interferon-gamma/genetics/*immunology/metabolism
;
Interleukin-10/genetics/metabolism
;
Leprosy, Lepromatous/genetics/*immunology/metabolism
;
Leprosy, Tuberculoid/genetics/*immunology/metabolism
;
Microbial Viability
;
Monocytes/immunology/metabolism
;
Mycobacterium leprae/*immunology/physiology
;
RNA, Messenger/genetics/metabolism
;
Receptors, Calcitriol/genetics/metabolism
;
Transcriptome
;
Tuberculosis/genetics/immunology
;
Up-Regulation
;
beta-Defensins/genetics/metabolism
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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