- Author(s): Pierre SAINT-MEZARD, Aurore ROSIERES, Maya KRASTEVA, Frédéric BERARD, Bertrand DUBOIS, Dominique KAISERLIAN, Jean-François NICOLAS
, INSERM U 503, IFR 128 Bioscience Lyon-Gerland, 21, avenue Tony Garnier 69007 Lyon, INSERM U 404, IFR 128 Bioscience Lyon-Gerland, 21, avenue Tony Garnier 69007 Lyon, Clinical Immunology and Allergy Unit, CH Lyon-Sud, 69495 Pierre-Benite Cedex, France., J.F. Nicolas, Fax: (+33) 478 861 528. E-mail: email@example.com
- Key words: haptens, CD8 T cells, CTL, CD4 regulatory T cells, tolerance, contact sensitivity, contact dermatitis
- Page(s) : 284-95
- Published in: 2004
Contact dermatitis is an inflammatory skin condition induced by exposure to an environmental agent. Eczema and dermatitis are used synonymously to denote a polymorphous pattern of skin inflammation characterized at least in its acute phase by erythema, vesiculation and pruritus. Substances responsible for contact dermatitis after single or multiple exposures are non protein chemicals, i.e. haptens, that induce skin inflammation through activation of innate skin immunity (irritant contact dermatitis) or both innate and acquired specific immunity (allergic contact dermatitis). The present review will focus on allergic contact dermatitis, a delayed-type hypersensitivity reaction, which is mediated by hapten-specific T cells. Recent advances in the pathophysiology of ACD have shown that the occurrence of ACD, as well as its magnitude and duration, is controlled by the opposite functions of CD8 effector T cells and CD4 regulatory T cells. From these studies ACD can be considered as a breakdown of cutaneous immune tolerance to haptens.