| First Author | Takeda K | Year | 1996 |
| Journal | Nature | Volume | 380 |
| Issue | 6575 | Pages | 627-30 |
| PubMed ID | 8602263 | Mgi Jnum | J:32561 |
| Mgi Id | MGI:80055 | Doi | 10.1038/380627a0 |
| Citation | Takeda K, et al. (1996) Essential role of Stat6 in IL-4 signalling. Nature 380(6575):627-30 |
| abstractText | Interleukin-4 (IL-4) is a pleiotropic lymphokine which plays an important role in the immune system. IL-4 activates two distinct signalling pathways through tyrosine phosphorylation of Stat6, a signal transducer and activator of transcription, and of a 170K protein called 4PS. To investigate the functional role of Stat6 in IL-4 signalling, we generated mice deficient in Stat6 by gene targeting. We report here that in the mutant mice, expression of CD23 and major histocompatibility complex (MHC) class II in resting B cells was not enhanced in response to IL-4. IL-4 induced B-cell proliferation costimulated by anti-IgM antibody was abolished. The T-cell proliferative response was also notably reduced. Furthermore, production of Th2 cytokines from T cells as well as IgE and IgG1 responses after nematode infection were profoundly reduced. These findings agreed with those obtained in IL-4 deficient mice or using antibodies to IL-4 and the IL-4 receptor. We conclude that Stat6 plays a central role in exerting IL-4 mediated biological responses. |
