ArticleFrontiers in immunology2026
RAG1 deficiency durably alters dermal group 2 innate lymphoid cells and modifies contact hypersensitivity.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Dermal group 2 innate lymphoid cells (dILC2s) contribute to skin homeostasis and inflammatory responses, yet they are frequently studied in Rag1-deficient mice in which the dILC2 compartment may itself be altered. Methods: We compared dILC2s from wild-type (WT) and Rag1-deficient mice by transcriptomic profiling, flow cytometric phenotyping, and functional analysis in a DNFB-induced contact hypersensitivity model with short-term adoptive lymphocyte transfer. Results: Rag1 deficiency was associated with a marked expansion of dILC2s and broad transcriptional remodeling, including increased expression of Il7r, Thy1, Il5, and Il13, together with enrichment of cytokine signaling, apoptosis, and activation pathways. Discussion: Together, these findings show that Rag1 deficiency durably alters dILC2 state and responsiveness and should be taken into account when interpreting cutaneous inflammation models in immunodeficient mice.
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