| First Author | Parker ME | Year | 2020 |
| Journal | J Exp Med | Volume | 217 |
| Issue | 1 | PubMed ID | 31570496 |
| Mgi Jnum | J:285229 | Mgi Id | MGI:6392670 |
| Doi | 10.1084/jem.20191030 | Citation | Parker ME, et al. (2020) c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program. J Exp Med 217(1) |
| abstractText | CCR6- group 3 innate lymphoid cells (ILC3s) are mediators of intestinal immunity and barrier function that possess the capacity to acquire type 1 effector features and fully convert into ILC1s. The molecular mechanisms governing such plasticity are undefined. Here, we identified c-Maf as an essential regulator of ILC3 homeostasis and plasticity that limits physiological ILC1 conversion. Phenotypic analysis of effector status in Maf-deficient CCR6- ILC3s, coupled with evaluation of global changes in transcriptome, chromatin accessibility, and transcription factor motif enrichment, revealed that c-Maf enforces ILC3 identity. c-Maf promoted ILC3 accessibility and supported RORgammat activity and expression of type 3 effector genes. Conversely, c-Maf antagonized type 1 programming, largely through restraint of T-bet expression and function. Mapping of the dynamic changes in chromatin landscape accompanying CCR6- ILC3 development and ILC1 conversion solidified c-Maf as a gatekeeper of type 1 regulatory transformation and a controller of ILC3 fate. |
