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Updated: Jun 25, 2025

Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
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Pathogenic Autoimmunity in Atherosclerosis Evolves from HSP60-Reactive CD4 + T Cells.

Shixiang Wang1, Yongquan Chen1, Danyan Zhou1

  • 1Department of Cardiology, The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou, 510150, China.

Journal of Cardiovascular Translational Research
|May 20, 2024
PubMed
Summary

Anti-heat shock protein 60 (HSP60) antibodies promote atherosclerosis (AS) by driving autoimmune responses. This study reveals anti-HSP60 autoimmunity exacerbates AS via macrophage infiltration and polarization, dependent on humoral immunity.

Keywords:
AtherosclerosisCD4 + T cellsHSP60M1 polarizationMacrophage

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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Autoimmunity

Background:

  • Clinical evidence links anti-HSP60 antibodies to atherosclerosis (AS) development.
  • The precise mechanisms underlying this association remain unclear.
  • Investigating anti-HSP60-mediated autoimmunity is crucial for understanding AS pathogenesis.

Purpose of the Study:

  • To elucidate the role of anti-HSP60 autoimmunity in the progression of atherosclerosis.
  • To characterize HSP60-specific T cell responses and their differentiation in AS.
  • To determine the impact of anti-HSP60 treatments on immune cell activity and plaque development.

Main Methods:

  • Utilized HSP60-MHC tetramers to identify and analyze HSP60-specific CD4+ T cells and T cell receptor (TCR) responses in mice.
  • Transplanted HSP60-reactive CD4+ T cells into AS mouse models to assess immune cell behavior in plaques and blood.
  • Administered recombinant HSP60 or anti-HSP60 sera to mice to evaluate effects on plaque progression and macrophage polarization.
  • Employed muMT-/-Apoe-/- mice to investigate the contribution of humoral immunity to anti-HSP60 autoimmunity.

Main Results:

  • HSP60-reactive CD4+ T cells in AS mice predominantly differentiated into follicular helper cells, not Th1 or Th17 subtypes.
  • Anti-HSP60 treatments led to increased macrophage infiltration and M1 polarization within atherosclerotic plaques.
  • These pro-inflammatory effects driven by anti-HSP60 were dependent on the presence of humoral immunity.
  • Experiments in muMT-/-Apoe-/- mice confirmed the critical role of humoral immunity in this autoimmune response.

Conclusions:

  • Anti-HSP60 autoimmunity significantly contributes to atherosclerosis progression.
  • The mechanism involves enhanced macrophage infiltration and M1 polarization, promoting inflammation.
  • Humoral immunity is essential for mediating the detrimental effects of anti-HSP60 autoimmunity in AS.
  • Targeting anti-HSP60-mediated autoimmune responses may offer a novel therapeutic strategy for atherosclerosis.