Ectopically expressed PIR-B on T cells constitutively binds to MHC class I and attenuates T helper type 1 responses

Michiyo Imada, Kyoko Masuda, Rumi Satoh, Yumi Ito, Yoshiyuki Goto, Takayuki Matsuoka, Shota Endo, Akira Nakamura, Hiroshi Kawamoto, Toshiyuki Takai

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

Activated mature T cells induce various inhibitory receptors implicated in maintaining peripheral tolerance in response to the trans -acting ligands. Interestingly, paired Ig-like receptor (PIR)-B, an inhibitory MHC class I receptor on B cells and myeloid cells, could be involved in regulating early T cell development because epitope for PIR is detected on pre-thymic T/NK progenitors but not on thymocytes or mature T cells. We hypothesized that PIR-B is not only a regulator for T cell development but is also detrimental if expressed on mature T cells. Here we demonstrated, using PIR-B-deficient fetuses, that PIR-B is indeed expressed on the T cell progenitors but failed to identify its distinctive roles in the development. Forced expression of PIR-B in thymocytes and mature T cells also resulted in no abnormalities in development. However, upon antigenic or allogeneic stimulation, peripheral T cells with the ectopic PIR-B showed reduced Th type 1 responses due to the suppression of proximal TCR signaling by constitutive binding of PIR-B to MHC class I on the same cell surface. Our findings suggest that T cell expression of PIR-B with the cis-interacting MHC class I is strictly prohibited in periphery so as to secure prompt immune responses.

Original languageEnglish
Pages (from-to)1151-1161
Number of pages11
JournalInternational immunology
Volume21
Issue number10
DOIs
Publication statusPublished - 2009

Keywords

  • Immunoregulatory receptor
  • T cell differentiation
  • T cell suppression
  • Tolerance

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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