| First Author | Doi K | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 425 |
| Issue | 1 | Pages | 107-12 |
| PubMed ID | 22828507 | Mgi Jnum | J:187164 |
| Mgi Id | MGI:5435625 | Doi | 10.1016/j.bbrc.2012.07.065 |
| Citation | Doi K, et al. (2012) ZFAT plays critical roles in peripheral T cell homeostasis and its T cell receptor-mediated response. Biochem Biophys Res Commun 425(1):107-12 |
| abstractText | ZFAT, originally identified as a candidate susceptibility gene for autoimmune thyroid disease, has been reported to be involved in apoptosis, development and primitive hematopoiesis. Zfat is highly expressed in T- and B-cells in the lymphoid tissues, however, its physiological function in the immune system remains totally unknown. Here, we generated the T cell-specific Zfat-deficient mice and demonstrated that Zfat-deficiency leads to a remarkable reduction in the number of the peripheral T cells. Intriguingly, a reduced expression of IL-7Ralpha and the impaired responsiveness to IL-7 for the survival were observed in the Zfat-deficient T cells. Furthermore, a severe defect in proliferation and increased apoptosis in the Zfat-deficient T cells following T cell receptor (TCR) stimulation was observed with a reduced IL-2Ralpha expression as well as a reduced IL-2 production. Thus, our findings reveal that Zfat is a critical regulator in peripheral T cell homeostasis and its TCR-mediated response. |
