| First Author | Kaplan MH | Year | 1996 |
| Journal | Immunity | Volume | 4 |
| Issue | 3 | Pages | 313-9 |
| PubMed ID | 8624821 | Mgi Jnum | J:31932 |
| Mgi Id | MGI:79436 | Doi | 10.1016/s1074-7613(00)80439-2 |
| Citation | Kaplan MH, et al. (1996) Stat6 is required for mediating responses to IL-4 and for development of Th2 cells. Immunity 4(3):313-9 |
| abstractText | Interleukin-4 (IL-4) stimulation of cells leads to the activation of multiple signaling pathways, one of which involves Stat6. We have generated Stat6-deficient mice by gene targeting in embryonic stem cells to determine the role of this transcription factor in mediating the biologic functions of IL-4. IL-4-induced increases in the cell surface expression of both MHC class II antigens and IL-4 receptor are completely abrogated, and lymphocytes from Stat6-deficient animals fail to proliferate in response to IL-4. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. In addition, Stat6-deficient T lymphocytes fail to differentiate into Th2 cells in response to either IL-4 or Il-13. These results demonstrate that, despite the existence of multiple signaling pathways activated by IL-4, Stat6 is essential for mediating responses to IL-4 lymphocytes. |
