miR-155 is significantly overexpressed in patients with atopic dermatitis and might contribute to chronic skin inflammation by increasing the proliferative response of T(H) cells through the downregulation of CTLA-4.
In this first study of its kind, we demonstrated directly that the observed inverse association between childhood eczema and type 1 diabetes is not likely to be explained by the established diabetes susceptibility genes HLA-DQ, CTLA4, or PTPN22.