Regulation of plasmacytoid dendritic cell responses by PIR-B

Yoshiya Mitsuhashi, Akira Nakamura, Shota Endo, Kazuya Takeda, Toshiki Yabe-Wada, Toshihiro Nukiwa, Toshiyuki Takai

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

Plasmacytoid dendritic cells (PDCs) produce type I interferons (IFNs) in response to viral nucleic acids to exert antiviral immunity. However, PDCs are related to the progress and severity of autoimmune diseases, such as systemic lupus erythematosus, because they respond to host DNA. Therefore, the regulation of PDC activation is critical for maintaining adequate immune responses. Here we show that an inhibitory major histocompatibility complex class I receptor, paired immunoglobulin-like receptor B (PIR-B), suppressed Fms-like tyrosine kinase 3 ligand-induced PDC differentiation in BM cells, as well as Toll-like receptor 9-mediated IFN-α production by PDCs, through the dephosphorylation of STAT1 STAT2. In particular, PIR-B inhibited IFN-α-mediated STAT phosphorylation, suggesting that PIR-B negatively regulates the positive feedback mechanism of IFN-α secretion triggered by Toll-like receptor 9. These results demonstrate a novel regulatory role for PIR-B in PDCs.

Original languageEnglish
Pages (from-to)3256-3259
Number of pages4
JournalBlood
Volume120
Issue number16
DOIs
Publication statusPublished - 2012 Oct 18

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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