| First Author | Zhang L | Year | 2021 |
| Journal | Cell Mol Immunol | Volume | 18 |
| Issue | 1 | Pages | 230-242 |
| PubMed ID | 32203192 | Mgi Jnum | J:361172 |
| Mgi Id | MGI:7737831 | Doi | 10.1038/s41423-020-0404-0 |
| Citation | Zhang L, et al. (2021) The transcription factor RelB restrains group 2 innate lymphoid cells and type 2 immune pathology in vivo. Cell Mol Immunol 18(1):230-242 |
| abstractText | The exact relationships between group 2 innate lymphoid cells (ILC2s) and Th2 cells in type 2 pathology, as well as the mechanisms that restrain the responses of these cells, remain poorly defined. Here we examined the roles of ILC2s and Th2 cells in type 2 lung pathology in vivo using germline and conditional Relb-deficient mice. We found that mice with germline deletion of Relb (Relb(-/-)) spontaneously developed prominent type 2 pathology in the lung, which contrasted sharply with mice with T-cell-specific Relb deletion (Relb(f/f)Cd4-Cre), which were healthy with no observed autoimmune pathology. We also found that in contrast to wild-type B6 mice, Relb-deficient mice showed markedly expanded ILC2s but not ILC1s or ILC3s. Moreover, adoptive transfer of naive CD4(+) T cells into Rag1(-/-)Relb(-/-) hosts induced prominent type 2 lung pathology, which was inhibited by depletion of ILC2s. Mechanistically, we showed that Relb deletion led to enhanced expression of Bcl11b, a key transcription factor for ILC2s. We concluded that RelB plays a critical role in restraining ILC2s, primarily by suppressing Bcl11b activity, and consequently inhibits type 2 lung pathology in vivo. |
