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Allergic contact dermatitis is an eczema precipitated by an exogenous agent, often a chemical, which is recognized by the immune system as an antigen and results in T-cell-mediated inflammation. Often, irritant and endogenous factors are also involved in the clinical picture.
Individual predisposition to allergic contact dermatitis varies. Similar exposures to chemicals in cosmetics, medicinal products or environmental allergens give rise to allergic reactivity in some and not in others. Certain people develop allergy following low-level exposure while in others, multiple hypersensitivities occur. However, there is little to support a genetic effect.
Induction of an allergic response is initiated through the skin. Chemical antigen is bound to self-proteins on, and processed by, skin dendritic cells, which migrate it to the draining lymph node for presentation to naive CD4+ T lymphocytes. Within 5–7 days or longer, these specific effector T cells leave the lymph node and return to the skin under skin-homing molecular control where, when the chemical allergen is re-encountered, inflammation is induced producing dermatitis.
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