Journal
CARDIOVASCULAR RESEARCH
Volume 102, Issue 1, Pages 107-117Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvu002
Keywords
Atherosclerosis; Regression; Inflammation; Lymphocytes; Regulatory T-cell
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Funding
- JSPS KAKENHI [24591114, 23790849, 25860601]
- Global Center of Excellence
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Mishima Kaiun Memorial Foundation
- Takeda Science Foundation
- Mitsui Life Social Welfare Foundation
- Yakult Bioscience Research Foundation
- Uehara Memorial Foundation
- Suzuken Memorial Foundation
- ONO Medical Research Foundation
- Grants-in-Aid for Scientific Research [24591114, 23790849, 25860601] Funding Source: KAKEN
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Aims Although recent animal studies have investigated the cellular and molecular mechanisms underlying the process of atherosclerosis regression, it remains unknown whether adaptive immune responses including T cells are involved in this process. We investigated the role of T cells in atherosclerosis regression. Methods and results LDL receptor-deficient mice were fed a high-cholesterol diet for 8 weeks to form atherosclerotic lesions and were then changed to a standard diet, and atherosclerosis was assessed 4 weekslater. Just before changing the diet, the mice received an iv injection of anti-CD3 antibody (CD3-Ab) or control immunoglobulin G for 5 consecutive days. CD3-Ab treatment regressed atherosclerosis and decreased the accumulation of macrophages and CD4(+) T cells in the plaques. CD3-Ab treatment also dramatically reduced CD4(+) T cells and increased the proportion of regulatory T cells (Tregs). Depletion of Tregs by anti-CD25 antibody injection abolished the regression of atherosclerosis seen in CD3-Ab-treated mice, indicating the essential role for Tregs in this process. Conclusion CD3-Ab treatment induced rapid regression of established atherosclerosis via reducing CD4(+) T cells and increasing the proportion of Tregs. These findings suggest that therapeutic intervention for T-cell-mediated immune responses may represent a novel strategy to induce atherosclerosis regression in combination with lipid-lowering therapy.
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