Sci. Signal., 26 March 2013
Immunology Interfering with Interferons
Kristen L. Mueller
Science, AAAS, Washington, DC 20005, USA
Infections with Mycobacteria, including Mycobacterium leprae or M. tuberculosis, vary substantially in their clinical presentation. For instance, in some cases of M. leprae, the infection is self-healing, with very few lesions. In contrast, some people experience the disseminated form, where skin lesions abound and bacteria are abundant. In patients infected with M. leprae, Teles et al. found that the disseminated disease associates with a type I interferon gene signature, whereas the self-healing form associates with a type II interferon gene signature. In cultured cells, type I interferon and its downstream signaling cascade inhibited the antimicrobial response induced by type II interferons, providing a potential explanation for why robust disease rather than protection is seen in some cases of infection.
R. M. B. Teles, T. G. Graeber, S. R. Krutzik, D. Montoya, M. Schenk, D. J. Lee, E. Komisopoulou, K. Kelly-Scumpia, R. Chun, S. S. Iyer, E. N. Sarno, T. H. Rea, M. Hewison, J. S. Adams, S. J. Popper, D. A. Relman, S. Stenger, B. R. Bloom, G. Cheng, R. L. Modlin, Type I interferon suppresses type II interferon–triggered human anti-mycobacterial responses. Science 339, 1448–1453 (2013). [Abstract] [Full Text]
Citation: K. L. Mueller, Interfering with Interferons. Sci. Signal. 6, ec75 (2013).
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