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.
Further studies revealed that inflammation severity correlated with switching TGFβ1 transgene expression on and off, and genome wide expression profiling revealed striking similarities between K5.TGFβ1 skin and human psoriasis, a Th1/Th17-associated inflammatory skin disease.