skinsensitization

Skin sensitization is an immunologically mediated adverse reaction of the skin to certain chemicals, resulting in allergic contact dermatitis in individuals who become sensitized. It is typically classified as a type IV hypersensitivity reaction, driven by hapten-protein adduct formation and T cell–mediated immune responses after dermal exposure.

The process includes an induction (sensitization) phase and an elicitation (challenge) phase. In induction, small reactive molecules called haptens covalently bind to skin proteins, creating hapten-protein adducts that are captured by Langerhans cells and other antigen-presenting cells. These cells migrate to draining lymph nodes and prime hapten-specific memory T cells. Upon re-exposure, elicitation occurs as memory T cells release cytokines and recruit inflammatory cells to the skin, producing dermatitis.

Common sensitizers include nickel, fragrances, epoxy resins, preservatives, and plant-derived urushiol. Nickel allergy is among the most prevalent forms. Clinically, allergic contact dermatitis presents as pruritic, erythematous, vesicular dermatitis at exposure sites, with onset typically 24–72 hours after re-exposure.

Regulatory science has increasingly favored non-animal methods. In vitro assays such as the direct peptide reactivity assay (DPRA) and cell-based tests like h-CLAT and ARE-Nrf2 luciferase assess sensitization potential, while in vivo options such as the local lymph node assay have declined in use. Patch testing in humans remains the standard clinical method to identify sensitizers in individuals.

Prevention focuses on avoidance of known sensitizers and appropriate protective measures, with product labeling and occupational controls. Management involves treating dermatitis and minimizing re-exposure to reduce relapse.