The Role of Interleukin-4 and Interleukin-12 in the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice

摘要: Accumulation of T cells and macrophages in atherosclerotic plaques the formation antibodies directed against plaque proteins suggests that adaptive immunity contributes to development atherosclerosis. The contribution Th1 Th2 helper cell subsets atherogenesis was studied a murine model by interbreeding apolipoprotein E-deficient (apoE−/−) mice with deficient key cytokines drive either responses [interleukin (IL)-12] or (IL-4). Compared apoE−/− mice, apoE−/−/IL-12−/− had 52% reduction area aortic root at 30 weeks age (P < 0.001). ApoE−/−/IL-4−/− 27% compared 0.05) age, but their were significantly larger than this stage 0.05). By 45 there no significant differences lesion sizes between strains, however apoE−/−/IL-4−/− showed 58% 64% decrease disease arch respectively, 78% thoracic lesions This both play roles throughout atherosclerosis various vascular sites mice.