Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice

Honglian Tong, Yoshiyuki Miyazaki, Masanori Yamazaki, Hiromitsu Hara, Herman Waldmann, Shohei Hori, Hiroki Yoshida

研究成果: Contribution to journalArticle査読

25 被引用数 (Scopus)

抄録

Epstein-Barr virus-induced gene-3 (EBI-3) associates with p28 to form interleukin-27 (IL-27) or with IL-12p35 to form IL-35. Both IL-27 and IL-35 have immunosuppressive functions and especially IL-35 has been implicated in the suppressive function of regulatory T cells (Treg). To address the role of EBI-3 in immune regulation, delayed-type hypersensitivity (DTH) responses were examined in EBI-3-deficient (EBI-3-/-) mice. EBI-3-/- mice developed deteriorated DTH responses as shown by the enhanced footpad swelling and augmented infiltration of inflammatory cells into the antigen-challenged footpads as compared with wild-type (WT) mice. While EBI-3-deficiency showed little effects on antigen-specific IFN-γ production of lymph node cells, IL-17 production was drastically augmented in EBI-3-/- cells as compared with in WT cells. In addition, reduced IL-10 production was also evident in EBI-3-/- CD4+ T cells. Interestingly, the development and suppressive function of Treg to inhibit effector T cell proliferation was not affected by EBI-3-deficiency. These data clearly demonstrated the immunosuppressive function of EBI-3 and provided complementary evidence that EBI-3 and EBI-3-containing cytokines might be taken into consideration as potential targets for some immune-related diseases.

本文言語英語
ページ(範囲)108-115
ページ数8
ジャーナルImmunology Letters
128
2
DOI
出版ステータス出版済み - 2 2010
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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