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

Abstract

T-cells expressing αE(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 αE(CD103) contributes to skin inflammation. Using two complementary approaches, we have investigated αE(CD103) in psoriasis-like skin inflammation of mice with transgenic epidermal expression of human TGFβ1: αE(CD103) was inhibited by function-blocking antibodies in vivo, and double-mutants with additional αE(CD103)-depletion were generated in two different genetic backgrounds. Epidermal hTGFβ1 expression was associated with prominent expression of αE(CD103) on infiltrating cells. However, neither treatment with αE(CD103)-blocking antibodies nor deficiency of αE(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 αE(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.