ArticleAnnals of the rheumatic diseases2015
Dysregulated CD4+ T cells from SLE-susceptible mice are sufficient to accelerate atherosclerosis in LDLr-/- mice.
Article in Annals of the rheumatic diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
- Is clonal haematopoiesis the missing link between lupus and cardiovascular disease?Rheumatology (Oxford, England) · 2026Review
- Immunopathogenesis of accelerated atherosclerosis in systemic lupus erythematosus: from innate and adaptive dysregulation to clinical implications.Frontiers in immunology · 2026Review
- The immunomodulatory potential of vitamin D on Th17 lymphocytes in systemic lupus erythematosus - a literature review.Medicine and pharmacy reports · 2025Review
- Systemic lupus erythematosus and atherosclerosis: immune pathways and the uncharted territory of gut microbiota and metabolism.Frontiers in immunology · 2025Review
- Autoimmune diseases and atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024Review
- Oxidized Phospholipid oxPAPC Alters Regulatory T-Cell Differentiation and Decreases Their Protective Function in Atherosclerosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Update of Potential Biomarkers in Risk Prediction and Monitoring of Atherosclerosis in Systemic Lupus Erythematosus to Prevent Cardiovascular Disease.Biomedicines · 2023Review
- Immunotherapy-Associated Atherosclerosis: A Comprehensive Review of Recent Findings and Implications for Future Research.Current treatment options in cardiovascular medicine · 2023Review
- The Intersection of Cellular and Systemic Metabolism: Metabolic Syndrome in Systemic Lupus Erythematosus.Endocrinology · 2022Review
- Cardiovascular disease risk and pathogenesis in systemic lupus erythematosus.Seminars in immunopathology · 2022Review
- Review
- Immunosenescence: an unexplored role in glomerulonephritis.Clinical & translational immunology · 2022Review
- Vascular Inflammation in Mouse Models of Systemic Lupus Erythematosus.Frontiers in cardiovascular medicine · 2022Article
- Endothelial Dysfunction in Systemic Lupus Erythematosus and Systemic Sclerosis: A Common Trigger for Different Microvascular Diseases.Frontiers in medicine · 2022Review
- Review
- The latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapy.Current opinion in rheumatology · 2021Review
- Naive CD8Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- T cells expressing the lupus susceptibility allele Pbx1d enhance autoimmunity and atherosclerosis in dyslipidemic mice.JCI insight · 2020Article
- T Cells in Autoimmunity-Associated Cardiovascular Diseases.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveAccelerated atherosclerosis is a major source of morbidity in systemic lupus erythematosus (SLE). However, the cause of SLE-accelerated atherosclerosis remains unclear.
methodsCD4(+) T cells from C57/Bl/6 (B6) or SLE-susceptible B6.Sle1.2.3 (B6.SLE) mice were transferred into LDLr(-/-), Rag(-/-) mice. T cells were examined for cytokine production and expression of interleukin-10 receptor (IL-10R) and functional markers. T cells were isolated based on FoxP3(GFP) expression and transferred to LDLr(-/-), Rag(-/-) mice to establish a role for B6.SLE effector T cells (Teff) in atherosclerosis.
resultsMice receiving whole B6.SLE CD4(+) T cells displayed no other SLE phenotype; however, atherosclerosis was increased nearly 40%. We noted dysregulated IL-17 production and reduced frequency of IL-10R expression by B6.SLE regulatory T cells (Treg). Functional assays indicated resistance of B6.SLE Teff to suppression by both B6.SLE and B6 Treg. Transfer experiments with CD4(+)FoxP3(-) Teff and CD4(+)FoxP3(+) Treg from B6.SLE and B6 mice, respectively, resulted in increased atherosclerosis compared with B6 Teff and Treg recipients. Treg isolated from mice receiving B6.SLE Teff with B6 Treg had increased production of IL-17 and fewer expressed IL-10R compared with B6 Teff and Treg transfer.
conclusionsTransfer of B6.SLE Teff to LDLr(-/-), Rag(-/-) mice results in accelerated atherosclerosis independent of the source of Treg. In addition, the presence of B6.SLE Teff resulted in more IL-17-producing Treg and fewer expressing IL-10R, suggesting that B6.SLE Teff may mediate phenotypic changes in Treg. To our knowledge, this is the first study to provide direct evidence of the role of B6.SLE Teff in accelerating atherosclerosis through resistance to Treg suppression.
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