Your browser doesn't support javascript.
loading
Interleukin-1α released from HSV-1-infected keratinocytes acts as a functional alarmin in the skin.
Milora, Katelynn A; Miller, Samantha L; Sanmiguel, Julio C; Jensen, Liselotte E.
Afiliação
  • Milora KA; Department of Microbiology and Immunology, Temple Autoimmunity Center, Temple University School of Medicine, 1158 MERB, 3500 N Broad Street, Philadelphia, Pennsylvania 19140, USA.
  • Miller SL; Department of Microbiology and Immunology, Temple Autoimmunity Center, Temple University School of Medicine, 1158 MERB, 3500 N Broad Street, Philadelphia, Pennsylvania 19140, USA.
  • Sanmiguel JC; Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania, TRL Building, 125 S 31st Street, Philadelphia, Pennsylvania 19104, USA.
  • Jensen LE; Department of Microbiology and Immunology, Temple Autoimmunity Center, Temple University School of Medicine, 1158 MERB, 3500 N Broad Street, Philadelphia, Pennsylvania 19140, USA.
Nat Commun ; 5: 5230, 2014 Oct 17.
Article em En | MEDLINE | ID: mdl-25323745
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-1ß (IL-1ß) in the intracellular space, which blocks the pro-inflammatory activity of IL-1ß. 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.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Pele / Queratinócitos / Herpesvirus Humano 1 / Interleucina-1alfa / Alarminas Limite: Animals / Humans Idioma: En Ano de publicação: 2014 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Pele / Queratinócitos / Herpesvirus Humano 1 / Interleucina-1alfa / Alarminas Limite: Animals / Humans Idioma: En Ano de publicação: 2014 Tipo de documento: Article