Allergic contact dermatitis (ACD) is a common inflammatory skin disease with a prevalence of approximately 20% in the European population. ACD is caused by contact allergens that are reactive chemicals able to modify non-immunogenic self-proteins to become immunogenic proteins. The most frequent contact allergens are metals, fragrances, and preservatives. ACD clinically manifests as pruritic eczematous lesions, erythema, local papules, and oedema. ACD is a T cell-mediated disease, involving both CD4+ and CD8+ T cells. In addition, γδ T cells appear to play an important role in the immune response to contact allergens. However, it is debated whether γδ T cells act in a pro- or anti-inflammatory manner. A special subset of γδ T cells, named dendritic epidermal T cells (DETC), is found in the epidermis of mice and it plays an important role in immunosurveillance of the skin. DETC are essential in sensing the contact allergen-induced stressed environment. Thus, allergen-induced activation of DETC is partly mediated by numerous allergen-induced stress proteins expressed on the keratinocytes (KC). Several stress proteins, like mouse UL-16-binding protein-like transcript 1 (Mult-1), histocompatibility 60 (H60) and retinoic acid early inducible-1 (Rae-1) α-ε family in mice and major histocompatibility complex (MHC) class I—chain-related A (MICA) in humans, are upregulated on allergen-exposed KC. Allergen-induced stress proteins expressed on the KC are consequently recognized by NKG2D receptor on DETC. This review focuses on the role of γδ T cells in ACD, with DETC in the spotlight, and on the role of stress proteins in contact allergen-induced activation of DETC.

Allergic contact dermatitis (ACD), an inflammatory dermatosis caused by contact of the skin with substances from the environment, is known to humankind since ancient times. One of the first cases come from the first century A.D., where patients experienced pruritic eczema upon cutting pine trees.

ACD is a type IV hypersensitivity mainly orchestrated by allergen-specific T cells, and it is one of the most frequent forms of inflammatory skin diseases. ACD clinically manifests as pruritic eczematous lesions, erythema, local papules and oedema. In most cases, the dermatitis is localized to the site of contact with the contact allergen; however, systemic reactions can also occur. In chronic lesions, the skin is scaly and thicker with erythema and often vesicles.

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