RORα-expressing T regulatory cells restrain allergic skin inflammation

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Science Immunology  02 Mar 2018:
Vol. 3, Issue 21, eaao6923
DOI: 10.1126/sciimmunol.aao6923

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Curbing ILC2 enthusiasm

Atopic dermatitis is an allergic disease driven by type 2 immune responses in the skin. Using mouse models of dermatitis, Malhotra et al. have identified tumor necrosis factor (TNF) family cytokine, TNF ligand–related molecule 1 (TL1A), and its receptor death receptor 3 (DR3) as being critical in regulating cross-talk between skin-resident T regulatory cells (Tregs) and type 2 innate lymphoid cells (ILC2) that drive skin inflammation. They report that retinoid-related orphan receptor α (RORα) drives expression of DR3 in Tregs and that, upon deletion of RORα, skin-resident Tregs are unable to sequester TL1A that drives effector functions of ILC2s. The studies open up the possibility of targeting the TL1A-DR3 in the context of dermatitis and other skin allergies.