Pathogenic Autoimmunity in Atherosclerosis Evolves from HSP60-Reactive CD4 + T Cells.

Autor: Wang S; Department of Cardiology, The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou, 510150, China., Chen Y; Department of Cardiology, The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou, 510150, China., Zhou D; Department of Cardiology, The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou, 510150, China., Zhang J; Department of Cardiology, The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou, 510150, China., Guo G; Department of Cardiology, The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou, 510150, China., Chen Y; Department of Cardiology, The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou, 510150, China. gzchenyouquan@163.com.
Jazyk: angličtina
Zdroj: Journal of cardiovascular translational research [J Cardiovasc Transl Res] 2024 Oct; Vol. 17 (5), pp. 1172-1180. Date of Electronic Publication: 2024 May 20.
DOI: 10.1007/s12265-024-10516-8
Abstrakt: Clinical evidence suggests anti-Hsp60 antibodies could contribute to atherosclerosis (AS) development, with unclear mechanisms. This study aims to explore the role of anti-HSP60-mediated autoimmunity in AS progression. HSP60-MHC tetramers were used to characterize HSP60-specific CD4 + T cells and assess TCR responses in mice. These cells were transplanted into AS mice to examine immune cell differentiation and infiltration in plaques and blood. Mice were injected with recombinant HSP60 or anti-HSP60 sera to evaluate effects on plaque progression and macrophage activity. Experiments with muMT -/- Apoe -/- mice examined humoral immunity's role in this autoimmunity. HSP60-reactive CD4 + T cells in AS mice differentiated into follicular helper cells, not Th1/Th17. Anti-HSP60 treatments increased macrophage infiltration and M1 polarization, indicating an anti-HSP60-driven inflammatory progression, dependent on humoral immunity. Anti-HSP60 influences macrophage infiltration, polarization, and plaque formation via humoral immunity, shedding light on its potential role in AS progression.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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