| First Author | Sciumé G | Year | 2012 |
| Journal | J Exp Med | Volume | 209 |
| Issue | 13 | Pages | 2331-8 |
| PubMed ID | 23209316 | Mgi Jnum | J:194630 |
| Mgi Id | MGI:5474425 | Doi | 10.1084/jem.20122097 |
| Citation | Sciume G, et al. (2012) Distinct requirements for T-bet in gut innate lymphoid cells. J Exp Med 209(13):2331-8 |
| abstractText | Interleukin (IL)-22-producing innate lymphoid cells (ILCs; ILC22) comprise a heterogeneous population of cells that are dependent on the transcription factor retinoid-related orphan gammat (RORgammat) and are critical for barrier function of the intestinal mucosa. A distinct ILC22 subset expresses the natural cytotoxicity receptor NKp46 (NKp46+ ILC22); however, the factors that contribute to the generation of this population versus other subsets are largely unknown. Herein, we show that T-bet (encoded by Tbx21) was highly expressed in NKp46+ ILC22, a feature shared by all NKp46+ cells present in the intestine but not by other IL-22-producing populations. Accordingly, the absence of T-bet resulted in loss of NKp46+ ILC22 in the intestinal lamina propria. The residual NKp46+ ILC22 present in Tbx21(-/-) mice showed a marked reduction of Rorgammat expression and impairment in IL-22 production. Generation and functions of gut NK1.1+ cells were also altered. Bone marrow chimera experiments revealed a cell-intrinsic requirement for T-bet in these subsets and competitive reconstitution experiments revealed roles for T-bet in multiple ILC subsets. Thus, T-bet has a general importance for ILC in the gut and plays a selective and critical role in the generation of NKp46+ ILC22. |
