| First Author | Fushimi S | Year | 2009 |
| Journal | Clin Immunol | Volume | 133 |
| Issue | 3 | Pages | 437-46 |
| PubMed ID | 19766538 | Mgi Jnum | J:155235 |
| Mgi Id | MGI:4413381 | Doi | 10.1016/j.clim.2009.08.015 |
| Citation | Fushimi S, et al. (2009) Forced expression of suppressor of cytokine signaling 3 in T cells protects the development of concanavalin A-induced hepatitis in mice. Clin Immunol 133(3):437-46 |
| abstractText | 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. |
