Topical glucocorticosteroids inhibit allergic skin inflammation but are ineffective in impeding the formation and expansion of resident memory T cells

Tissue-resident memory T (TRM) cells are detrimental in numerous chronic inflammatory diseases, including allergic contact dermatitis (ACD), in which they contribute to the chronicity and severity of the disease. We assessed the impact of a standard glucocorticosteroid treatment, triamcinolone acetonide (TA), on the formation, maintenance and reactivation of epidermal TRM cells in ACD. We used an experimental model of ACD to 2,4-dinitrofluorobenzene, that is mediated by allergen-specific CD8+ T cells. TA 0.01% was applied at different time points of CHS response and we monitored skin inflammation and tracked CD8+CD69+CD103 TRM by flow cytometry and RNA sequencing