Interferon-ε protects the female reproductive tract from viral and bacterial infection
Date
2013
Authors
Fung, K.
Mangan, N.
Cumming, H.
Horvat, J.
Mayall, J.
Stifter, S.
De Weerd, N.
Roisman, L.
Rossjohn, J.
Robertson, S.
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Journal article
Citation
Science, 2013; 339(6123):1088-1092
Statement of Responsibility
Ka Yee Fung, Niamh E. Mangan, Helen Cumming, Jay C. Horvat, Jemma R. Mayall, Sebastian A. Stifter, Nicole De Weerd, Laila C. Roisman, Jamie Rossjohn, Sarah A. Robertson, John E. Schjenken, Belinda Parker, Caroline E. Gargett, Hong P. T. Nguyen, Daniel J. Carr, Philip M. Hansbro, Paul J. Hertzog
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Abstract
The innate immune system senses pathogens through pattern-recognition receptors (PRRs) that signal to induce effector cytokines, such as type I interferons (IFNs). We characterized IFN-ε as a type I IFN because it signaled via the Ifnar1 and Ifnar2 receptors to induce IFN-regulated genes. In contrast to other type I IFNs, IFN-ε was not induced by known PRR pathways; instead, IFN-ε was constitutively expressed by epithelial cells of the female reproductive tract (FRT) and was hormonally regulated. Ifn-ε–deficient mice had increased susceptibility to infection of the FRT by the common sexually transmitted infections (STIs) herpes simplex virus 2 and Chlamydia muridarum. Thus, IFN-ε is a potent antipathogen and immunoregulatory cytokine that may be important in combating STIs that represent a major global health and socioeconomic burden.
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