| First Author | Yagi R | Year | 2014 |
| Journal | Immunity | Volume | 40 |
| Issue | 3 | Pages | 378-88 |
| PubMed ID | 24631153 | Mgi Jnum | J:210327 |
| Mgi Id | MGI:5570497 | Doi | 10.1016/j.immuni.2014.01.012 |
| Citation | Yagi R, et al. (2014) The transcription factor GATA3 is critical for the development of all IL-7Ralpha-expressing innate lymphoid cells. Immunity 40(3):378-88 |
| abstractText | Innate lymphoid cells (ILCs) are critical in innate immune responses to pathogens and lymphoid organ development. Similar to CD4(+) T helper (Th) cell subsets, ILC subsets positive for interleukin-7 receptor alpha (IL-7Ralpha) produce distinct sets of effector cytokines. However, the molecular control of IL-7Ralpha(+) ILC development and maintenance is unclear. Here, we report that GATA3 was indispensable for the development of all IL-7Ralpha(+) ILC subsets and T cells but was not required for the development of classical natural killer cells. Conditionally Gata3-deficient mice had no lymph nodes and were susceptible to Citrobactor rodentium infection. After the ILCs had fully developed, GATA3 remained important for the maintenance and functions of ILC2s. Genome-wide gene expression analyses indicated that GATA3 regulated a similar set of cytokines and receptors in Th2 cells and ILC2s, but not in ILC3s. Thus, GATA3 plays parallel roles in regulating the development and functions of CD4(+) T cells and IL-7Ralpha(+) ILCs. |
