Interferon-epsilon protects the female reproductive tract from viral and bacterial infection

Ka Yee Fung; Niamh Mangan; Helen Elizabeth Cumming; Jay C Horvat; Jemma R Mayall; Sebastian Anton Stifter; Nicole Anne De Weerd; Laila Catalina Roisman; Jamie Rossjohn; Sarah A Roberston; John E Schjenken; Belinda S Parker; Caroline Eve Gargett; Hong Phuong Thi Nguyen; Daniel J J Carr; Phillip M Hansbro; Paul John Hertzog

doi:10.1126/science.1233321

Interferon-epsilon protects the female reproductive tract from viral and bacterial infection

Ka Yee Fung, Niamh Mangan, Helen Elizabeth Cumming, Jay C Horvat, Jemma R Mayall, Sebastian Anton Stifter, Nicole Anne De Weerd, Laila Catalina Roisman, Jamie Rossjohn, Sarah A Roberston, John E Schjenken, Belinda S Parker, Caroline Eve Gargett, Hong Phuong Thi Nguyen, Daniel J J Carr, Phillip M Hansbro, Paul John Hertzog

Research output: Contribution to journal › Article › Research › peer-review

191 Citations (Scopus)

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-e 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-e was not induced by known PRR pathways; instead, IFN-e was constitutively expressed by epithelial cells of the female reproductive tract (FRT) and was hormonally regulated. Ifn-e-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-e is a potent antipathogen and immunoregulatory cytokine that may be important in combating STIs that represent a major global health and socioeconomic burden.

Original language	English
Pages (from-to)	1088 - 1092
Number of pages	5
Journal	Science
Volume	339
Issue number	6123
DOIs	https://doi.org/10.1126/science.1233321
Publication status	Published - 2013

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Fung, K. Y., Mangan, N., Cumming, H. E., Horvat, J. C., Mayall, J. R., Stifter, S. A., De Weerd, N. A., Roisman, L. C., Rossjohn, J., Roberston, S. A., Schjenken, J. E., Parker, B. S., Gargett, C. E., Nguyen, H. P. T., Carr, D. J. J., Hansbro, P. M., & Hertzog, P. J. (2013). Interferon-epsilon protects the female reproductive tract from viral and bacterial infection. Science, 339(6123), 1088 - 1092. https://doi.org/10.1126/science.1233321

@article{d841ef2b45c54cb98429c9d8fd66148a,

title = "Interferon-epsilon protects the female reproductive tract from viral and bacterial infection",

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-e 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-e was not induced by known PRR pathways; instead, IFN-e was constitutively expressed by epithelial cells of the female reproductive tract (FRT) and was hormonally regulated. Ifn-e-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-e is a potent antipathogen and immunoregulatory cytokine that may be important in combating STIs that represent a major global health and socioeconomic burden.",

author = "Fung, {Ka Yee} and Niamh Mangan and Cumming, {Helen Elizabeth} and Horvat, {Jay C} and Mayall, {Jemma R} and Stifter, {Sebastian Anton} and {De Weerd}, {Nicole Anne} and Roisman, {Laila Catalina} and Jamie Rossjohn and Roberston, {Sarah A} and Schjenken, {John E} and Parker, {Belinda S} and Gargett, {Caroline Eve} and Nguyen, {Hong Phuong Thi} and Carr, {Daniel J J} and Hansbro, {Phillip M} and Hertzog, {Paul John}",

year = "2013",

doi = "10.1126/science.1233321",

language = "English",

volume = "339",

pages = "1088 -- 1092",

journal = "Science",

issn = "0036-8075",

publisher = "American Association for the Advancement of Science (AAAS)",

number = "6123",

}

Fung, KY, Mangan, N, Cumming, HE, Horvat, JC, Mayall, JR, Stifter, SA, De Weerd, NA, Roisman, LC, Rossjohn, J, Roberston, SA, Schjenken, JE, Parker, BS, Gargett, CE, Nguyen, HPT, Carr, DJJ, Hansbro, PM & Hertzog, PJ 2013, 'Interferon-epsilon protects the female reproductive tract from viral and bacterial infection', Science, vol. 339, no. 6123, pp. 1088 - 1092. https://doi.org/10.1126/science.1233321

TY - JOUR

T1 - Interferon-epsilon protects the female reproductive tract from viral and bacterial infection

AU - Fung, Ka Yee

AU - Mangan, Niamh

AU - Cumming, Helen Elizabeth

AU - Horvat, Jay C

AU - Mayall, Jemma R

AU - Stifter, Sebastian Anton

AU - De Weerd, Nicole Anne

AU - Roisman, Laila Catalina

AU - Rossjohn, Jamie

AU - Roberston, Sarah A

AU - Schjenken, John E

AU - Parker, Belinda S

AU - Gargett, Caroline Eve

AU - Nguyen, Hong Phuong Thi

AU - Carr, Daniel J J

AU - Hansbro, Phillip M

AU - Hertzog, Paul John

PY - 2013

Y1 - 2013

N2 - 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-e 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-e was not induced by known PRR pathways; instead, IFN-e was constitutively expressed by epithelial cells of the female reproductive tract (FRT) and was hormonally regulated. Ifn-e-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-e is a potent antipathogen and immunoregulatory cytokine that may be important in combating STIs that represent a major global health and socioeconomic burden.

AB - 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-e 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-e was not induced by known PRR pathways; instead, IFN-e was constitutively expressed by epithelial cells of the female reproductive tract (FRT) and was hormonally regulated. Ifn-e-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-e is a potent antipathogen and immunoregulatory cytokine that may be important in combating STIs that represent a major global health and socioeconomic burden.

UR - http://www.ncbi.nlm.nih.gov/pubmed/23449591

U2 - 10.1126/science.1233321

DO - 10.1126/science.1233321

M3 - Article

SN - 0036-8075

VL - 339

SP - 1088

EP - 1092

JO - Science

JF - Science

IS - 6123

ER -

Interferon-epsilon protects the female reproductive tract from viral and bacterial infection

Abstract

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