| First Author | Hsiao HW | Year | 2009 |
| Journal | Immunity | Volume | 31 |
| Issue | 1 | Pages | 72-83 |
| PubMed ID | 19592273 | Mgi Jnum | J:151605 |
| Mgi Id | MGI:4354486 | Doi | 10.1016/j.immuni.2009.04.017 |
| Citation | Hsiao HW, et al. (2009) Deltex1 is a target of the transcription factor NFAT that promotes T cell anergy. Immunity 31(1):72-83 |
| abstractText | The molecular process underlying T cell anergy is incompletely understood. Deltex1 (DTX1) is a Notch target with unknown physiological function. Here we show that Dtx1 was a transcription target of nuclear factor of activated T cells (NFAT) and participated in T cell anergy. DTX1 protein was upregulated during T cell anergy, and transgenic expression of Dtx1 attenuated T cell activation. DTX1 inhibited T cell activation by both E3-dependent and E3-independent mechanisms. In addition, DTX1 suppressed T cell activation in the absence of its Notch-binding domain. Importantly, DTX1 regulated the expression of two anergy-associated molecules, growth arrest and DNA-damage-inducible 45 beta (Gadd45 beta) and Cbl-b. DTX1 interacted with early growth response 2 (Egr-2) for optimum expression of Cbl-b. Furthermore, deficiency of DTX1 augmented T cell activation, conferred resistance to anergy induction, enhanced autoantibody generation, and increased inflammation. DTX1 therefore represents a component downstream of calcium-NFAT signaling that regulates T cell anergy. |
