Atheroprotective Immunity and Interleukin-10 Linked to Reduced Characteristics of Plaque Stability
Autoimmunity to low-density lipoprotein (LDL) is linked to atherosclerosis, with LDL immunization proposed as a preventive measure, but the mechanisms of atheroprotective immunity are not well understood. We investigated T-cell responses to LDL using 2 T-cell receptor transgenic mouse strains. At 52 weeks, BT1×HuBL mice showed reduced atherosclerosis, increased humoral responses against LDL, and lower plasma cholesterol. Conversely, BT3×HuBL mice had reduced atherosclerosis without changes in cholesterol, linked to increased type 1 regulatory T cells, interleukin (IL)-10 production, and decreased characteristics of plaque stability. In human plaques, IL10 mRNA negatively correlated with collagen content, and IL-10 inhibited collagen production in vitro. We conclude that atheroprotective LDL immunity elicits 2 distinct pathways: lipid-lowering immune responses and local anti-inflammatory IL-10 production. Because IL-10 is associated with decreased plaque stability and increased risk of cardiovascular events, treatments aimed at promoting IL-10 signaling over extended periods to reduce vascular inflammation should be carefully monitored.
LDL; T-lymphocyte; adaptive immunity; apolipoprotein B-100; atherosclerosis; cardiovascular disease; lipoproteins.
Copyright © 2025 The Authors. Published by Elsevier Inc. All rights reserved.
Funding Support and Author Disclosures This work was supported by grants from the Swedish Heart-Lung Foundation (20180523, 20210469, and 20230391), the Swedish Research Council (2020-01789), Åke Wibergs Stiftelse, Foundation for Age Research at Karolinska Institutet, Professor Nanna Svartz Foundation, Jeansson Foundation, Magnus Bergvall Foundation, Gun and Bertil Stohne Foundation, Loo and Hans Osterman Foundation, Stiftelsen för Gamla Tjänarinnor, King Gustav Vth and Queen Victoria Foundation, and Karolinska Institutet. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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