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Allergic contact dermatitis (ACD) is a common inflammatory skin disorder characterized as a T cell-mediated delayed-type hypersensitivity reaction induced by cutaneous exposure to haptens. Its pathogenesis unfolds through three distinct phases: sensitization, elicitation, and resolution. During sensitization, hapten-modified proteins are processed by dendritic cells, particularly Langerhans cells and dermal dendritic cells, which migrate to lymph nodes to prime naive T cells. Pattern recognition receptors, including Toll-like receptors and the NLRP3 inflammasome, critically regulate this innate-adaptive interface. The elicitation phase involves hapten-specific Th1 and Th17 cells orchestrating inflammation through cytotoxicity and cytokine release. Conversely, resolution relies on regulatory T cells and IL-10 and TGF-beta signaling to restore tissue homeostasis. Emerging immunomodulators such as vitamin D exhibit dose-dependent regulatory effects potentially influenced by sex-specific factors and U-shaped associations. Despite significant advances, critical gaps persist regarding tissue-resident memory T cells and precise sensitization thresholds. Integrating immunology, neurobiology, and metabolomics may advance precision therapies targeting pathways like NLRP12 or ultraviolet-induced vitamin D synthesis. This review summarizes current progress in elucidating the immunopathogenesis of ACD and highlights emerging mechanisms that may support the development of more precise and effective therapeutic strategies.
Tong et al. (Wed,) studied this question.