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Skin-Infiltrating CD8⁺ T Cells Initiate Atopic Dermatitis Lesions¹

Ana Hennino^*,, Marc Vocanson^*,, Yann Toussaint^*,, Karen Rodet^*,, Josette Benetière^*,, Anne-Marie Schmitt, Marie-Françoise Aries, Frédéric Bérard^*,,, Aurore Rozières^*,, and Jean-François Nicolas^2,*,,

^* Institut National de la Santé et de la Recherche Médicale, Unité 503, L’Institut Fédératif de Recherche 128 BioSciences Lyon-Gerland, and Université Claude Bernard Lyon 1, Lyon, France; Hospices Civils de Lyon, Department of Clinical Immunology and Allergy, Centre Hospitalier Universitaire de Lyon Sud, Pierre Bénite, France; and Institut de Recherche Pierre Fabre, Hôtel Dieu St-Jacques, Toulouse, France

Skin lesions in the allergic form of atopic dermatitis (AD) are induced by allergen-specific T cells that infiltrate the skin at the site of allergen exposure. Although Th2-type CD4⁺ T cells appear to be crucial in AD pathophysiology, little is known about the contribution of CD8⁺ T cells in the development of the allergic skin inflammation. In the present study, we have analyzed the respective role of CD8⁺ and CD4⁺ T cells in the development of AD skin lesions in a mouse model of allergen-induced AD. In sensitized mice, CD8⁺ T cells are rapidly and transiently recruited to the allergen-exposed site and initiate the inflammatory process leading to skin infiltration with eosinophils and Th1/Th2-producing cells. CD8⁺ T cell-depleted mice show no inflammation, demonstrating that these cells are mandatory for the development of AD. In contrast, CD4⁺ T cell-depleted mice develop a severe form of eczema. Furthermore, adoptive transfer of CD8⁺ T cells from sensitized mice into naive recipient mice leads to skin inflammation soon after allergen exposure. These data indicate that allergen-primed CD8⁺ T cells are required for the development of AD-like lesions in mice.

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¹ This work was supported by institutional grants from Institut National de la Santé et de la Recherche Médicale, Université Claude Bernard Lyon 1, and Hospices Civils de Lyon and by a grant from the Centre de Recherche sur la Peau et les Épithélium de Revêtement, Pierre Fabre Laboratories (Castres, France).

² Address correspondence and reprint requests to Dr. Jean-François Nicolas, Institut National de la Santé et de la Recherche Médicale Unité 503, L’Institut Fédératif de Recherche 128, 21 av Tony Garnier, 69375 Lyon, France. E-mail address: jean-francois.nicolas{at}chu-lyon.fr or nicolas{at}cervi-lyon.inserm.fr

³ Abbreviations used in this paper: AD, atopic dermatitis; FasL, Fas ligand; CLA, cutaneous lymphocyte-associated Ag; Der f, Dermatophagoides farinae; Der p, Dermatophagoides pteronyssinus; LN, lymph node; SFC, spot-forming cell; TARC, thymus- and activation-regulated chemokine.