074 Newly identification of a CXCR6+ pathogenic skin-resident CD4+ T cell subset in a mouse model of allergic dermatitis that requires CXCL16 for its maintenance

CD4+ tissue-resident memory T (TRM) cells persist in the skin after an allergic reaction and induce rapid inflammation upon antigen re-exposure. However, mechanisms underlying maintenance of TRM their functional heterogeneity remain largely unknown. To clarify this, we first used a delayed-type hypersensitivity model with adaptive transfer ovalbumin (OVA)-specific using cell receptor-β deficient mice as recipients. Mice were sensitized OVA emulsion then challenged ear (day 0). On day 35, when swelling had resolved, remained dermis CD44+CD69+ phenotype. Consistently, parabiosis experiments confirmed tissue residency. Immunohistochemical analysis revealed that formed clusters CD301b+ dermal dendritic cells. address importance its interaction, selectively depleted CD301b-diphtheria toxin receptor mice, found number decreased depletion. In addition, depletion reduced transcription level CXC-chemokine ligand 16 (CXCL16). And receptor, 6 (CXCR6), was preferentially expressed on We blocking CXCL16 inhibited proliferation CXCR6+CD4+ attenuated re-challenge. Finally, RNA-sequencing produced IFN-γ IL-13 re-challenge, whereas CXCR6-CD4+ displayed Foxp3+ regulatory Taken together, these results indicate play pathogenic role during recall responses by producing effector cytokines, is mediated interacting via CXCL16. This mechanism provides new strategy for preventing recurrence chronic diseases, such atopic dermatitis.