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Interleukin-1α released from HSV-1-infected keratinocytes acts as a functional alarmin in the skin

Author

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  • Katelynn A. Milora

    (Temple Autoimmunity Center, Temple University School of Medicine)

  • Samantha L. Miller

    (Temple Autoimmunity Center, Temple University School of Medicine)

  • Julio C. Sanmiguel

    (Gene Therapy Program, University of Pennsylvania)

  • Liselotte E. Jensen

    (Temple Autoimmunity Center, Temple University School of Medicine)

Abstract

Herpes simplex virus-1 (HSV-1) is a human pathogen that utilizes several strategies to circumvent the host immune response. An immune evasion mechanism employed by HSV-1 is retention of interleukin-1β (IL-1β) in the intracellular space, which blocks the pro-inflammatory activity of IL-1β. Here we report that HSV-1-infected keratinocytes actively release the also pro-inflammatory IL-1α, preserving the ability of infected cells to signal danger to the surrounding tissue. The extracellular release of IL-1α is independent of inflammatory caspases. In vivo recruitment of leukocytes to early HSV-1 microinfection sites within the epidermis is dependent upon IL-1 signalling. Following cutaneous HSV-1 infection, mice unable to signal via extracellular IL-1α exhibit an increased mortality rate associated with viral dissemination. We conclude that IL-1α acts as an alarmin essential for leukocyte recruitment and protective immunity against HSV-1. This function may have evolved to counteract an immune evasion mechanism deployed by HSV-1.

Suggested Citation

  • Katelynn A. Milora & Samantha L. Miller & Julio C. Sanmiguel & Liselotte E. Jensen, 2014. "Interleukin-1α released from HSV-1-infected keratinocytes acts as a functional alarmin in the skin," Nature Communications, Nature, vol. 5(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6230
    DOI: 10.1038/ncomms6230
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