Skin-Infiltrating CD8+ T Cells Initiate Atopic Dermatitis Lesions

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 dev...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of immunology (1950) Vol. 178; no. 9; pp. 5571 - 5577
Main Authors Hennino, Ana, Vocanson, Marc, Toussaint, Yann, Rodet, Karen, Benetiere, Josette, Schmitt, Anne-Marie, Aries, Marie-Francoise, Berard, Frederic, Rozieres, Aurore, Nicolas, Jean-Francois
Format Journal Article
LanguageEnglish
Published United States Am Assoc Immnol 01.05.2007
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary: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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.178.9.5571