SOCS1 regulates type I/type II NKT cell balance by regulating IFNγ signaling

Masayuki Hashimoto, Kiyokazu Hiwatashi, Kenji Ichiyama, Rimpei Morita, Takashi Sekiya, Akihiro Kimura, Yuki Sugiyama, Toshikatsu Sibata, Kazumichi Kuroda, Reiko Takahashi, Akihiko Yoshimura

研究成果: Article査読

17 被引用数 (Scopus)

抄録

Suppressor of cytokine signaling-1 (SOCS1) has been shown to be an essential negative regulator of cytokine responses, including those of IFNγ, IL-2, IL-4 and IL-7. SOCS1 deficiency resulted in hyperactivation not only of T cells in general but also of NKT cells specifically. Consistent with previous reports, T- and NKT-cell-specific deletion of Socs1 in mice resulted in enhanced sensitivity to ConA-induced hepatitis. Compared with wild-type (WT) NKT cells, SOCS1-deficient NKT cells produced larger quantities of IFNγg in response to ConA and proliferated faster in response to IL-2 and IL-15. To our surprise, however, SOCS1-deficient NKT cells did not respond to the synthetic glycolipid ligand alpha-galactosylceramide (α-GalCer), though they did respond to sulfatide. α-GalCer-CD1d-tetramer-positive type I NKT [invariant NKT (iNKT)] cells were marginally detected in the periphery of SOCS1-conditional knockout (cKO) mice, suggesting that most of the SOCS1-deficient NKT cells at the periphery were type II NKT cells. Consistently, invariant Vα14 expression was much lower in SOCS1-deficient NKT cells than in WT NKT cells, indicating that iNKT cell homeostasis was abnormal in SOCS1-cKO mice. This reduction in iNKT cells was not observed in mice of an IFNγ-deficient background. These results suggest that SOCS1 is an important regulator of the balance between type I and type II NKT cells at the periphery.

本文言語English
ページ(範囲)165-176
ページ数12
ジャーナルInternational immunology
23
3
DOI
出版ステータスPublished - 2011 3月 1

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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