Authors
Omid Dadoo, B Sumayyah H Sokeechand, Anna Lee, Mark T Fuller, Yu Chang David Wang, Melissa E MacDonald, Nicole L Batenburg, Suleiman A Igdoura, Carl D Richards, Ali A Ashkar, Bernardo L Trigatti
Published in
Frontiers in physiology. Volume 17. Pages 1859434. Epub Aug 04, 2026.
Abstract
Interleukin (IL)-15 is essential for the survival and maturation of natural killer (NK) and CD8+ T cells, and it directly activates macrophages.
In the present study, we examined the effects of inactivating Il-15 on atherosclerosis in apolipoprotein (apo) E-deficient mice.
As 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.
PMID:
42614258
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.
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