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Updated: Jun 17, 2026

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
Published on: September 26, 2022
Drug hypersensitivity reactions involving skin
Oliver Hausmann1, Benno Schnyder, Werner J Pichler
1Division of Allergology, Department of Rheumatology, Clinical Immunology and Allergology, Inselspital, CH-3010 Bern, Switzerland.
Delayed drug hypersensitivity reactions involve T cells, not just IgE. The p-i concept explains how drugs can directly interact with T cell receptors, leading to diverse immune responses and clinical symptoms.
Area of Science:
- Immunology
- Pharmacology
- Dermatology
Background:
- Drug hypersensitivity reactions range from immediate IgE-mediated responses to delayed T cell-mediated reactions.
- Delayed reactions manifest hours to days after drug initiation, affecting various organs and potentially leading to fatal systemic diseases.
- T cells play a crucial role in delayed drug hypersensitivity, with both CD4+ and CD8+ T cells recognizing drugs via their T cell receptors (TCR).
Purpose of the Study:
- To elucidate the mechanisms underlying T cell-mediated delayed drug hypersensitivity.
- To introduce and explain the pharmacological interaction of drugs with immune receptors (p-i) concept.
- To explore how distinct T cell functions contribute to the diverse clinical phenotypes of drug hypersensitivity.
Main Methods:
- Immunohistochemical and functional studies of drug-specific T cells in patients.
- Analysis of T cell receptor (TCR) interactions with drugs and major histocompatibility complex (MHC) molecules.
- Subclassification of delayed hypersensitivity reactions based on T cell cytokine and chemokine profiles.
Main Results:
- Confirmed the predominant role of T cells in delayed drug hypersensitivity (type IV reactions).
- Proposed two drug stimulation models: hapten-carrier and the novel p-i concept involving non-covalent TCR binding.
- Demonstrated that distinct T cell functions, mediated by specific cytokines/chemokines, lead to subclassification into type IVa (monocyte), IVb (eosinophil), and IVd (neutrophil) reactions.
Conclusions:
- The p-i concept provides a framework for understanding how drugs can directly activate T cells, explaining frequent skin manifestations.
- Diverse clinical presentations of T cell-mediated drug hypersensitivity are linked to specific T cell effector functions.
- Subclassification of type IV reactions into IVa, IVb, and IVd refines our understanding of immune cell involvement in drug hypersensitivity.
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