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• W2790717594 abstract "Atherosclerosis is a chronic inflammatory disease characterized by the entrapment of apolipoprotein B–containing lipoproteins in the arterial intima, leading to local inflammation. T helper (Th) cell 1–mediated immune responses have been associated with atherosclerosis, and the cytokine interleukin-25 (IL-25 or IL-17E) has been reported to potentially regulate Th1 cell– and Th17 cell–related immune responses. In this study, we evaluated the effects of complete IL-25 deficiency or of a temporal IL-25 blockade on atherosclerosis development in apolipoprotein E–deficient (Apoe−/−) mice. Mice deficient in both apolipoprotein E and IL-25 (Apoe−/−/IL-25−/−) had more Th1 cells in the spleen, along with elevated plasma levels of IL-17 and an increased release of splenic interferon-γ (INF-γ). In support of this observation, a 4-week-long treatment of young Apoe−/− mice (at 10–14 weeks of age) with an IL-25–blocking antibody increased the release of Th1/Th17-associated cytokines in the spleen. In both mouse models, these findings were associated with increased atherosclerotic plaque formation in the aortic arch. We conclude that complete IL-25 deficiency and a temporal IL-25 blockade during early plaque development aggravate atherosclerosis development in the aortic arch of Apoe−/− mice, accompanied by an increase in Th1/Th17-mediated immune responses. Our finding that endogenous IL-25 has an atheroprotective role in the murine aortic arch has potential implications for atherosclerosis development and management in humans. Atherosclerosis is a chronic inflammatory disease characterized by the entrapment of apolipoprotein B–containing lipoproteins in the arterial intima, leading to local inflammation. T helper (Th) cell 1–mediated immune responses have been associated with atherosclerosis, and the cytokine interleukin-25 (IL-25 or IL-17E) has been reported to potentially regulate Th1 cell– and Th17 cell–related immune responses. In this study, we evaluated the effects of complete IL-25 deficiency or of a temporal IL-25 blockade on atherosclerosis development in apolipoprotein E–deficient (Apoe−/−) mice. Mice deficient in both apolipoprotein E and IL-25 (Apoe−/−/IL-25−/−) had more Th1 cells in the spleen, along with elevated plasma levels of IL-17 and an increased release of splenic interferon-γ (INF-γ). In support of this observation, a 4-week-long treatment of young Apoe−/− mice (at 10–14 weeks of age) with an IL-25–blocking antibody increased the release of Th1/Th17-associated cytokines in the spleen. In both mouse models, these findings were associated with increased atherosclerotic plaque formation in the aortic arch. We conclude that complete IL-25 deficiency and a temporal IL-25 blockade during early plaque development aggravate atherosclerosis development in the aortic arch of Apoe−/− mice, accompanied by an increase in Th1/Th17-mediated immune responses. Our finding that endogenous IL-25 has an atheroprotective role in the murine aortic arch has potential implications for atherosclerosis development and management in humans." @default.
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• W2790717594 date "2018-05-01" @default.
• W2790717594 modified "2023-10-18" @default.
• W2790717594 title "Interleukin-25 (IL-25) has a protective role in atherosclerosis development in the aortic arch in mice" @default.
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• W2790717594 doi "https://doi.org/10.1074/jbc.ra117.000292" @default.
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