In another animal model, NC/Nga mice, RvE1 reduced the development of AD-like skin lesions induced by 2,4-dinitrofluorobenzene (DNFB) treatment by suppressing the production of IL-4 and IFN-γ by activated CD4+T cells, and by decreasing lesional infiltration by CD+4, CD8+ T cells, as well as the mast cells and eosinophils, in addition to suppression of total serum IgE levels [86]. The gene discussed is CD4; the disease is Alzheimer disease.