1. ¹IFR 128 BioSciences Lyon-Gerland, Institut National de la Santé et de la Recherche Médicale (INSERM) U503, Lyon Cedex, France
2. ²Department of Allergy and Clinical Immunology, Pierre Benite, France
3. ³IFR 128 BioSciences Lyon-Gerland, INSERM U404, Lyon Cedex, France

Correspondence: Dr Jean-François Nicolas, INSERM U503, IFR 128, 21 av Tony Garnier, 69375 Lyon Cx 07, France. E-mail: jean-francois.nicolas@chu-lyon.fr or nicolas@cervi-lyon.inserm.fr

Received 31 May 2005; Revised 13 October 2005; Accepted 2 November 2005; Published online 2 February 2006.

Abstract

Allergic contact dermatitis (ACD) to strong experimental haptens is mediated by specific CD8+ T cells. Here, we show that similar mechanisms occur for weak haptens, which comprise the vast majority of chemicals responsible for human ACD. We used a model of ACD, that is, the contact hypersensitivity reaction, to test for the allergenicity of three weak haptens involved in fragrance allergy. ACD to weak haptens could not be induced in normal mice. In contrast, mice acutely depleted in CD4+ T cells developed a typical ACD reaction to the three weak fragrance allergens that peaked 24 hours after challenge. Priming of CD8+ T cells was observed in draining lymph nodes 5 days after sensitization and development of ACD was associated with the infiltration of activated CD8+ T cells in the challenged skin. CD8+ T cells were effectors of the ACD reaction as in vivo treatment with depleting anti-CD8 mAbs abrogated the ACD responses and as purified CD8+ T cells could adoptively transfer ACD to naive recipients. In conclusion, our data demonstrate a dominant role of CD8+ T cells as initiators of ACD to weak haptens, and suggest that CD8+ T cells may represent potential targets for preventing or treating ACD.