| First Author | Hashimoto M | Year | 2011 |
| Journal | Int Immunol | Volume | 23 |
| Issue | 3 | Pages | 165-76 |
| PubMed ID | 21393632 | Mgi Jnum | J:169668 |
| Mgi Id | MGI:4941642 | Doi | 10.1093/intimm/dxq469 |
| Citation | Hashimoto M, et al. (2011) SOCS1 regulates type I/type II NKT cell balance by regulating IFN{gamma} signaling. Int Immunol 23(3):165-76 |
| abstractText | Suppressor of cytokine signaling-1 (SOCS1) has been shown to be an essential negative regulator of cytokine responses, including those of IFNgamma, 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 IFNgamma 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 (alpha-GalCer), though they did respond to sulfatide. alpha-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 Valpha14 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 IFNgamma-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. |
