| First Author | Cai Q | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 4 | Pages | 2303-11 |
| PubMed ID | 19620299 | Mgi Jnum | J:151553 |
| Mgi Id | MGI:4354434 | Doi | 10.4049/jimmunol.0901407 |
| Citation | Cai Q, et al. (2009) Helios deficiency has minimal impact on T cell development and function. J Immunol 183(4):2303-11 |
| abstractText | Helios is a member of the Ikaros family of zinc finger transcription factors. It is expressed mainly in T cells, where it associates with Ikaros-containing complexes and has been proposed to act as a rate-limiting factor for Ikaros function. Overexpression of wild-type or dominant-negative Helios isoforms profoundly alters alphabeta T cell differentiation and activation, and endogenous Helios is expressed at strikingly high levels in regulatory T cells. Helios has also been implicated as a tumor suppressor in human T cell acute lymphoblastic leukemias. These studies suggest a central role for Helios in T cell development and homeostasis, but whether this protein is physiologically required in T cells is unclear. We report herein that inactivation of the Helios gene by homologous recombination does not impair the differentiation and effector cell function of alphabeta and gammadelta T cells, NKT cells, and regulatory T cells. These results suggest that Helios is not essential for T cells, and that its function can be compensated for by other members of the Ikaros family. |
