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Updated: May 11, 2026

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
Published on: September 26, 2022
Characterization of the T cell response in allergic contact dermatitis caused by corticosteroids
Marie Baeck1, Angèle Soria, Liliane Marot
1Department of Dermatology, Cliniques Universitaires Saint-Luc, Universite' Catholique de Louvain, 1200 Brussels, Belgium. marie.baeck@uclouvain.be
Background:
Delayed allergic hypersensitivity reactions have classically been described as type IV reactions, which are caused by T cells; however, the respective roles of CD4(+) and CD8(+) cells are yet to be defined. A central role for CD8(+) cytotoxic T cells as effector cells has been suggested.
Objectives:
To determine the type of T cell involved in corticosteroid allergy.
Methods:
We analysed the kinetics of T cell recruitment and the cytokine production profile in positive patch tests of 27 corticosteroid-sensitized patients, as compared with control sites and control subjects. Skin biopsies, collected at 8, 24 and 48 hr following drug application, were embedded in paraffin for histological and immunohistological staining, and, in some cases, also deep-frozen for gene expression analyses.
Results:
CD3(+) T cells were rapidly recruited in concert with the positivity of the patch test sites. High levels of interleukin (IL)-4, IL-5 and, to a lesser extent, interferon-γ suggested that both Th2 and Th1 cytokines were implicated. IL-4 was also produced by γδ T cell receptor (TCR) lymphocytes.
Conclusions:
This study showed that, in allergic contact dermatitis caused by corticosteroids, the inflammatory infiltrate is composed of CD3(+) T cells with a predominant Th2 cytokine profile, among which IL-4 is also produced by γδ TCR lymphocytes.
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