@article{23853,
  keywords = {25-Hydroxyvitamin D3 1-alpha-Hydroxylase, Antimicrobial Cationic Peptides, Humans, Interferon-beta, Interferon-gamma, Interleukin-10, Leprosy, lepromatous, Leprosy, Tuberculoid, Microbial Viability, Monocytes, Mycobacterium leprae, RNA, Messenger, Receptors, Calcitriol, Transcriptome, Tuberculosis, Up-Regulation, Beta-Defensins},
  author = {Teles R and Graeber T and Krutzik SR and Montoya DJ and Schenk M and Lee DJ and Komisopoulou E and Kelly-Scumpia K and Chun R and Iyer S and Sarno E and Rea T and Hewison M and Adams J and Popper SJ and Relman D and Stenger S and Bloom B and Cheng G and Modlin RL},
  title = {Type I interferon suppresses type II interferon-triggered human anti-mycobacterial responses.},
  abstract = {<p>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.</p>},
  year = {2013},
  journal = {Science (New York, N.Y.)},
  volume = {339},
  pages = {1448-53},
  month = {2013 Mar 22},
  issn = {1095-9203},
  doi = {10.1126/science.1233665},
  language = {eng},
}