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

研究成果: Article査読

9 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)1151-1161
ページ数11
ジャーナルInternational Immunology
21
10
DOI
出版ステータスPublished - 2009
外部発表はい

All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学

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