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© Research
Publication : Immunity

Transcription factor Tox2 is required for metabolic adaptation and tissue residency of ILC3 in the gut.

Team: Meta-organism
Member: Nicolas Bouladoux
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Immunity - 14 May 2024

Das A, Martinez-Ruiz GU, Bouladoux N, Stacy A, Moraly J, Vega-Sendino M, Zhao Y, Lavaert M, Ding Y, Morales-Sanchez A, Harly C, Seedhom MO, Chari R, Awasthi P, Ikeuchi T, Wang Y, Zhu J, Moutsopoulos NM, Chen W, Yewdell JW, Shapiro VS, Ruiz S, Taylor N, Belkaid Y, Bhandoola A

Link to Pubmed [PMID] – 38677292

Link to DOI – 10.1016/j.immuni.2024.04.001

Immunity 2024 May; 57(5): 1019-1036.e9

Group 3 innate lymphoid cells (ILC3) are the major subset of gut-resident ILC with essential roles in infections and tissue repair, but how they adapt to the gut environment to maintain tissue residency is unclear. We report that Tox2 is critical for gut ILC3 maintenance and function. Gut ILC3 highly expressed Tox2, and depletion of Tox2 markedly decreased ILC3 in gut but not at central sites, resulting in defective control of Citrobacter rodentium infection. Single-cell transcriptional profiling revealed decreased expression of Hexokinase-2 in Tox2-deficient gut ILC3. Consistent with the requirement for hexokinases in glycolysis, Tox2-/- ILC3 displayed decreased ability to utilize glycolysis for protein translation. Ectopic expression of Hexokinase-2 rescued Tox2-/- gut ILC3 defects. Hypoxia and interleukin (IL)-17A each induced Tox2 expression in ILC3, suggesting a mechanism by which ILC3 adjusts to fluctuating environments by programming glycolytic metabolism. Our results reveal the requirement for Tox2 to support the metabolic adaptation of ILC3 within the gastrointestinal tract.