The contribution of interleukin-1β (IL-1β) signaling to the function of epidermal tissue-resident memory T (TRM) cells in allergic contact dermatitis (ACD) remains insufficiently defined. ACD is a T cell–mediated inflammatory skin disease, which is induced upon exposure of the skin to contact allergens (Vocanson et al., 2009). Nickel is the most prevalent contact allergen in humans and repeated exposure to nickel at the same skin site promotes a progressive enrichment of CD4+, CD8+ and regulatory TRM cells within the epidermis (Yeung et al., 2026).

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