Requirement of the IFN-α/β-induced CXCR3 chemokine signalling for CD8+ T cell activation

Kouetsu Ogasawara, Shigeaki Hida, Youmin Weng, Akio Saiura, Kojiro Sato, Hiroshi Takayanagi, Shinya Sakaguchi, Taeko Yokochi, Tatsuhiko Kodama, Makoto Naitoh, Julie A. De Martino, Tadatsugu Taniguchi

研究成果: Article査読

59 被引用数 (Scopus)

抄録

Background: Activation of both CD4+T and CD8+T cells is triggered by the engagement of the T cell antigen receptor (TCR) with MHC/peptide complexes on antigen-presenting cells. This process also requires other molecular interactions, which transmit co-stimulatory signals to these T cells. To ensure an effective immune response, distinct T cell subsets may additionally employ unique mechanism(s) for efficient activation. Results: We here show that mutant CD8+ T cells lacking the IFN-α/β signalling components are hyporesponsive to antigen stimulation in vitro. We further show that IFN-α/β-mediated signals are required for induction of the chemokines IP-10/ITAC and their common receptor, CXCR3, and in turn provide evidence that CXCR3-mediated signals indeed function in the activation and proliferation of CD8+ T cells, particularly for the CD44low naive phenotype cells. Conclusion: The CXCR3 chemokine system is regulated by IFN-α/β in CD8+T cells, and it is critical for the efficient cell activation. The present study therefore reveals a novel role of the IFN-α/β-CXCR3 signalling cascade in CD8+T cell activation.

本文言語English
ページ(範囲)309-320
ページ数12
ジャーナルGenes to Cells
7
3
DOI
出版ステータスPublished - 2002
外部発表はい

ASJC Scopus subject areas

  • 遺伝学
  • 細胞生物学

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