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

Katelynn A. Milora, Samantha L. Miller, Julio C. Sanmiguel and Liselotte E. Jensen ()
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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

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms6230

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