Allergic contact dermatitis is a frequently observed dermatosis, especially in industrialized countries. Regarded as a classical type IV immune reaction (delayed type), the process can be separated into two pathogenetic parts: the induction phase where sensitization takes place and the elicitation phase in which inflammation is induced upon re-exposure to the same antigen. A murine model was established decades ago, which reliably reproduces both phases. Epicutaneously applied low-molecular-weight sensitizers bind to proteins (haptens) and become full antigens, which results in sensitization. Subsequent administration of the same hapten onto ear skin causes a swelling response. This reaction is antigen specific because it cannot be induced in nonsensitized mice or in sensitized mice with a different hapten. This model was used to study the mechanisms involved in allergic contact dermatitis and also was intensively utilized to study immunologic mechanisms, including antigen presentation and development of T effector or regulatory T cells. The model’s major merit is its antigen specificity. It is highly reproducible, reliable, and simple to perform. In this paper, the methods of this technique are described to help researchers successfully establish this widely used model in laboratories. Describing the complex pathomechanisms underlying the model is beyond the scope of this article.
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