A novel regulatory role of gp49B on dendritic cells in T-cell priming

Satoshi Kasai, Masanori Inui, Kyohei Nakamura, Yuta Kakizaki, Shota Endo, Akira Nakamura, Sadayoshi Ito, Toshiyuki Takai

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)


Dendritic cells (DC) play pivotal roles in the induction and regulation of both innate and acquired immunity. DC express several cell-surface immune inhibitory receptors. However, little is known about their potential immunoregulatory functions in the context of T-cell activation. Here we report that murine gp49B, a member of the immunoglobulin superfamily, harboring immunoreceptor tyrosine-based inhibitory motifs, is expressed on DC and downregulates cellular activity to prevent the excessive activation of T cells in vitro and in vivo. Bone marrow-derived DC (BMDC) from newly generated gp49B-deficient (gp49B-/-) mice induced enhanced proliferation and IL-2 release of antigen-specific CD4+ and CD8+ T cells compared with BMDC from wild-type mice, in a cell-cell contact manner. The enhanced proliferation by gp49B-/- BMDC was also observed in allogeneic CD4+ and CD8+ T cells. Moreover, the transfer of allogeneic BALB/c splenocytes into C57BL/6 gp49B-/- mice induced severe acute graft-versus-host disease with an augmented upregulation of CD86 on CD11c+ splenic gp49B-/- DC, while transfer of C57BL/6 gp49B-/- splenocytes into BALB/c mice did not, suggesting the exacerbation of the disease was due, at least in part, to augmented activation of recipient gp49B-/- DC. These findings demonstrate a novel regulatory role of gp49B in the function of DC.

Original languageEnglish
Pages (from-to)2426-2437
Number of pages12
JournalEuropean Journal of Immunology
Issue number9
Publication statusPublished - 2008 Sep
Externally publishedYes


  • Antigen presentation
  • Costimulation
  • DC
  • Regulatory receptor
  • Tolerance

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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