| First Author | Park C | Year | 2000 |
| Journal | Immunity | Volume | 13 |
| Issue | 6 | Pages | 795-804 |
| PubMed ID | 11163195 | Mgi Jnum | J:66564 |
| Mgi Id | MGI:1928625 | Doi | 10.1016/s1074-7613(00)00077-7 |
| Citation | Park C, et al. (2000) Immune response in Stat2 knockout mice. Immunity 13(6):795-804 |
| abstractText | Type I IFNs induce gene expression through Stat1 and Stat2, which can in turn associate either to form Stat1 homodimers or the transcription factor ISGF-3. Stat1 homodimers also transduce signals for IFN-gamma. To explore the unique properties of Stat2 and ISGF-3 in type I IFN signaling, its gene was targeted for deletion. Stat2 null mice exhibit a number of defects in immune response. This includes an increased susceptibility to viral infection and the loss of a type I IFN autocrine/ paracrine loop, which in turn regulates several aspects of immune response. Intriguingly, Stat2-deficient fibroblasts exhibit a more significant defect in their response to type I IFNs than macrophages, highlighting tissue-specific differences in the response to this family of ligands. |
