Chemical-Induced Contact Hypersensitivity in the Mouse Model

Abstract

Hypersensitivity reactions to drugs most commonly manifest in skin. Like chemical-or metal ion-induced allergic contact dermatitis and contact hypersensitivity, most acute adverse drug reactions are mediated by cytotoxic T cells and controlled by immunosuppressive regulatory T cells. In both cases, progress has been made in the identification of the recognition structures for T cells and of the effector and regulatory mechanisms of disease, especially with respect to the adaptive immune response. However, a crucial, yet poorly understood event in these hypersensitivities is the activation of the innate immune system and the subsequent induction and polarization of the adaptive immune response. Recent findings in this field using the mouse contact hypersensitivity model will be discussed here. Future challenges are similar for the management of drug-and chemical-induced hypersensitivities. Thus, great efforts are being made to develop reliable in vitro assay systems for predictive risk assessment. The success of this research in assay development is tightly linked to progress in basic research that will not only lead to a more detailed understanding of the pathomechanisms, but also to the development of new treatments for these clinically and economically increasingly important hypersensitivity reactions.

Anti‐inflammatory and immune‐regulatory mechanisms prevent contact hypersensitivity to Arnica montana L.

“…Our data demonstrate the crucial role of the innate immune response that results in inflammation in CHS (36,37). Studies in mice as well as clinical studies demonstrate a strong potential of a variety of steroidal and non‐steroidal anti‐inflammatory drugs that reduce or prevent sensitization or elicitation of CHS following topical or systemic application.…”

The Role and Diagnosis of Allergic Contact Dermatitis in Patients with Atopic Dermatitis

“…However, Th2, Th17, and Th22 responses appear to play a role in ACD, sometimes depending on the allergen. [43][44][45] For example, nickel was found to be a potent inducer of the innate immune Th1, Th17, and Th22 pathways, while fragrance and rubber promoted Th2 activity with less Th1 and Th17 involvement. [46] IL-9 expression has also been found to be elevated in skin from positive patch-test reactions in ACD patients, including reactions to metals, drugs, and polymers; IL-9 also increased in nickel-allergic patients after nickel stimulation.…”