TCDD aggravates the formation of the atherosclerotic plaque in ApoE KO mice with a sexual dimorphic pattern.

Aryl hydrocarbon receptor (AhR) ligands are recognized as aggravating factors in cardiovascular diseases but little is known about the role of the AhR in atherosclerosis considering the effects of age and gender. We exposed male and female ApoE knock-out mice, a model to study the pathogenesis of atherosclerosis, to a potent AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by an intraperitoneal injection of 1 μg/kg/week for 8 weeks. Atherosclerotic lesions, histological parameters and critical atherosclerotic markers in aorta were analysed.

Control of the T follicular helper-germinal center B-cell axis by CD8⁺ regulatory T cells limits atherosclerosis and tertiary lymphoid organ development.

Background: The atheromodulating activity of B cells during the development of atherosclerosis is well documented, but the mechanisms by which these cells are regulated have not been investigated.

Methods And Results: Here, we analyzed the contribution of Qa-1-restricted CD8(+) regulatory T cells to the control of the T follicular helper-germinal center B-cell axis during atherogenesis. Genetic disruption of CD8(+) regulatory T cell function in atherosclerosis-prone apolipoprotein E knockout mice resulted in overactivation of this axis in secondary lymphoid organs, led to the increased development of tertiary lymphoid organs in the aorta, and enhanced disease development.