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Comment
. 2022 Feb;19(2):142-144.
doi: 10.1038/s41423-021-00816-3. Epub 2022 Jan 7.

Transcriptional control of mature ILC3 function and plasticity: not just RORγt

Xinping Lv  1 , Shan Zhu  1 , Jing Wu  1 , Jingtao Chen  2
Affiliations
Comment

Transcriptional control of mature ILC3 function and plasticity: not just RORγt

Xinping Lv et al. Cell Mol Immunol. 2022 Feb.
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Roles of coexpressed transcription factors in the identity and plasticity of ILCs. In LTi-like ILC3s, deletion of RORγt alone or together with RORα can lead to the loss of most biomarkers and functions of LTi-like ILC3s, but the core IL-22-producing capacity of ILC3s is maintained (upper left). In NCR+ ILC3s, RORγt can inhibit the transition of NCR+ ILC3s toward ex-ILC3s or ILC1s by antagonizing T-bet. When both RORγt and T-bet are deleted, RORα still sustains the IL-22-producing function and identity of ILC3s as unknown dysregulated ILC3s (upper right). The table below shows the ILC subset proportion change upon deletion of different combined transcription factors. ILC3, group 3 innate lymphoid cell; LTi, lymphoid tissue inducer; RORγt, retinoic acid receptor-related orphan receptorγt; NCR: natural cytotoxicity receptor
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