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Inactivation of interleukin-15 reduces spontaneous atherosclerosis in apolipoprotein E-deficient mice
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DOI：10.3389/fphys.2026.1859434.png)
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Abstract
En 中文
IntroductionInterleukin (IL)-15 is essential for the survival and maturation of natural killer (NK) and CD8+ T cells; and it directly activates macrophages.MethodsIn the present study; we examined the effects of inactivating Il-15 on atherosclerosis in apolipoprotein (apo) E-deficient mice.Results and discussionAs expected; Il-15 deficiency reduced circulating NK and CD8+ T cells in ApoE−/− mice. It also increased body weights in female but not male ApoE−/− mice and increased plasma total cholesterol levels in both. Despite this; the Il-15 knockout reduced spontaneous atherosclerotic plaque development in both male and female ApoE−/− mice (fed a normal diet) at 25 weeks of age; and in female normal diet-fed ApoE−/− mice at 15 weeks but not at 38 weeks of age. Furthermore; Il-15 knockout did not impact the levels of atherosclerosis in 25-week-old female ApoE−/− mice fed a high-fat; high-cholesterol diet for 15 weeks. However; the 6-week treatment with an antibody (M96) that blocks IL-15’s interaction with the IL-2Rβγc complex but does not interfere with its interaction with IL-15Rα reduced spontaneous atherosclerosis in female ApoE−/− mice. ApoE knockout mice in which IL-15 was inactivated or neutralized with an antibody exhibited reduced accumulation of CD11b+ and CD8+ cells within atherosclerotic plaques. These findings demonstrate that interfering with IL-15 signaling through the IL-2Rβγc complex delays spontaneous atherosclerosis development in ApoE-deficient mice.
Keywords:
inflammation
atherosclerosis
knockout mouse
interleukin-15 (IL-15)
antibody-based therapeutic
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