Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
|Title:||Interferon-ε protects the female reproductive tract from viral and bacterial infection|
|Other Titles:||Interferon-epsilon protects the female reproductive tract from viral and bacterial infection|
De Weerd, N.
|Citation:||Science, 2013; 339(6123):1088-1092|
|Publisher:||Amer Assoc Advancement Science|
|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|
|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.|
|Keywords:||Uterus; Vagina; Cell Line; Animals; Mice, Inbred C57BL; Humans; Mice; Chlamydia muridarum; Herpesvirus 2, Human; Chlamydia Infections; Herpes Genitalis; Interferons; Oligodeoxyribonucleotides; Poly dA-dT; Poly I-C; Estrogens; Ligands; Female; Toll-Like Receptors; HEK293 Cells|
|Rights:||Copyright status unknown|
|Appears in Collections:||Obstetrics and Gynaecology publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.