Integrin αE(CD103) is induced but plays no pathogenic role in psoriasiform skin lesions of TGFβ1 transgenic mice

Abstract

T-cells expressing α_E(CD103), an integrin induced by TGFβ on T-cells in vitro, accumulate within epithelia in inflammatory disorders, including psoriasis. However, it is unclear, if and how α_E(CD103) contributes to skin inflammation.

Using two complementary approaches, we have investigated α_E(CD103) in psoriasis-like skin inflammation of mice with transgenic epidermal expression of human TGFβ1: α_E(CD103) was inhibited by function-blocking antibodies in vivo, and double-mutants with additional α_E(CD103)-depletion were generated in two different genetic backgrounds.

Epidermal hTGFβ1 expression was associated with prominent expression of α_E(CD103) on infiltrating cells. However, neither treatment with α_E(CD103)-blocking antibodies nor deficiency of α_E(CD103) in double-mutant mice altered the psoriasis-like phenotype. In addition, histopathological and flow cytometric analyses revealed similar pathological skin alterations and lymphocyte subgroups in the different mouse strains. Thus, while α_E(CD103) expression is indeed associated with hTGFβ1 in vivo, it has little, if any, influence on the course of the psoriasis-like phenotype in K5.hTGFβ1-transgenic mice.

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