Low-dose interferon-α accelerates atherosclerosis in an LDL receptor-deficient mouse model
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摘要
Background: Solid evidence suggests that atheroscleosis is associated with immune reactions. Most of the activated T cells in the plaque are T helper 1 subtype (Th1), which secrete interferon-γ (IFN-γ), now generally accepted as a proatherogenic cytokine. Interferon-α (IFN-α) has been found to inhibit the secretion of IL-12 and IFN-γ and to increase IL-10 production. It may, therefore, be atheroprotective. The aim of the present study was to clarify the effect of IFN-α on atherogenesis in a transgenic mouse model of atherosclerosis. Methods: 8-week-old low-density lipoprotein (LDL) receptor-deficient mice were allocated randomly into treatment and control groups (n

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