Forced expression of suppressor of cytokine signaling 3 in T cells protects the development of concanavalin A-induced hepatitis in mice

Soichiro Fushimi, Tetsuya Ogino, Junko Hara, Tomohiro Takahata, Hiroshi Wakabayashi, Haruyuki Watanabe, Yasuharu Arashima, Masato Kubo, Akihiro Matsukawa

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8 Citations (Scopus)


T cells play central roles in liver diseases, but the regulatory mechanism by cytokine signaling is not well understood. In the present study, we explored the role of SOCS3 in T cells in concanavalin A (ConA)-induced hepatitis. Mice with T-cell-specific overexpression of SOCS3 (SOCS3-cTg) showed reduced hepatic damage and improved mice survival relative to the control, an event that was associated with decreased apoptotic signals Fas and pStat1. Expression of Th1-cytokines/chemokines was decreased in SOCS3-cTg liver with reduced expression of T-bet, a Th1-transcription factor. Flow cytometric analysis of the liver lymphocytes demonstrated that activated CD4+ T cells, cytotoxic T cells and natural killer T cells were significantly decreased in SOCS3-cTg liver with decreased expression of perforin and granzyme B, injurious molecules for hepatocyte damage. These results suggest that forced expression of SOCS3 in T cells prevents ConA-induced liver injury by inhibiting several phases of Th1 responses.

Original languageEnglish
Pages (from-to)437-446
Number of pages10
JournalClinical Immunology
Issue number3
Publication statusPublished - Dec 1 2009



  • Concanavalin A;
  • Fas;
  • Hepatotoxicity;
  • NKT cells;
  • SOCS;
  • T cells;
  • Th1 cytokine;
  • Transcription factor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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