dsRNA-mediated innate immunity of epidermal keratinocytes

Mikiko Tohyama, Xiuju Dai, Koji Sayama, Kenshi Yamasaki, Yuji Shirakata, Yasushi Hanakawa, Sho Tokumaru, Yoko Yahata, Lujun Yang, Hiroshi Nagai, Akira Takashima, Koji Hashimoto

Research output: Contribution to journalArticlepeer-review

39 Citations (Scopus)


MIP-1α, a CC chemokine, recruits monocytes, natural killer cells, lymphocytes, and neutrophils, and plays a critical role in viral infection. Since, the lesional epidermis of herpes zoster expressed MIP-1α, we hypothesized that keratinocytes produce MIP-1α in response to virus-associated dsRNA via TLR3. To investigate this, we examined cultured human keratinocytes for MIP-1α production induced by poly(I:C), a TLR3 ligand. Poly(I:C) treatment induced MIP-1α production, interestingly, poly(I:C)-induced IFN-α and -β production preceded MIP-1α production. A neutralizing antibody for IFN-β significantly inhibited the poly(I:C)-induced MIP-1α production indicating that MIP-1α production is via IFN-β. IFN-α priming enhanced TLR3 expression and MIP-1α production in poly(I:C)-treated keratinocytes. This suggests that IFN-α enhanced the TLR3 expression and reinforced the response of keratinocytes to poly(I:C), which resulted in an increase in MIP-1α production. In conclusion, normal human keratinocytes produce MIP-1α in response to dsRNA via TLR3, and this production is regulated by IFN-α/β.

Original languageEnglish
Pages (from-to)505-511
Number of pages7
JournalBiochemical and biophysical research communications
Issue number2
Publication statusPublished - 2005 Sept 23
Externally publishedYes


  • Herpes virus
  • IFN-α
  • IFN-β
  • Keratinocyte
  • MIP-1α
  • Skin
  • Viral infection

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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