| First Author | Kamezaki K | Year | 2004 |
| Journal | Int Immunol | Volume | 16 |
| Issue | 8 | Pages | 1173-9 |
| PubMed ID | 15226272 | Mgi Jnum | J:91540 |
| Mgi Id | MGI:3047445 | Doi | 10.1093/intimm/dxh118 |
| Citation | Kamezaki K, et al. (2004) The role of Tyk2, Stat1 and Stat4 in LPS-induced endotoxin signals. Int Immunol 16(8):1173-9 |
| abstractText | Mice lacking Tyk2, Stat1 or Stat4, which are members of the Jak-Stat signaling cascade, were resistant to LPS-induced endotoxin shock. Interestingly, Tyk2-deficient mice had higher resistance to LPS challenge than mice lacking either Stat1 or Stat4. The activation of MAPK and NF-kappaB by LPS, and the production of TNF-alpha and IL-12 after LPS injection, were not abrogated by the absence of Tyk2, Stat1 or Stat4. In Stat1-deficient mice, the induction of IFN-beta by LPS in macrophages was severely reduced, although the serum level of IFN-gamma was elevated after LPS injection. In contrast, in Stat-4 deficient mice, the induction of IFN-beta by LPS was normal, but the serum level of IFN-gamma remained low after LPS injection. Interestingly, the induction of both IFN-beta and IFN-gamma by LPS was severely reduced in Tyk2-deficient mice. Therefore, Stat1 and Stat4 independently play substantial roles in the susceptibility to LPS. Tyk2 is essential for LPS-induced endotoxin shock, and this signaling pathway is transduced by the activation of Stat1 and Stat4. |
