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Cytotoxic CD8+ T Cells Are Involved in the Thrombo-Inflammatory Response during First-Diagnosed Atrial Fibrillation

Julian Friebel1,2,3,4, Marco Witkowski1,5, Max Wegner1

  • 1Charité Center 11-Department of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 12203 Berlin, Germany.

Cells
|January 8, 2023
PubMed

Insights

Thrombin receptor (PAR1) signaling links blood clotting and inflammation via CD8+ T cells in early atrial fibrillation (AF). Targeting this pathway may reduce cardiovascular events in AF patients.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Hematology

Background:

  • Atrial myopathy and atrial fibrillation (AF) are linked to thrombo-inflammation, accelerating disease and major adverse cardiovascular events (MACEs).
  • Protease-activated receptor 1 (PAR1) signaling is key in mediating thrombo-inflammation.
  • This study investigates PAR1's role in linking coagulation and inflammation via cytotoxic CD8+ T cells in patients with first-diagnosed AF (FDAF).

Purpose of the Study:

  • To investigate the hypothesis that PAR1 signaling connects coagulation and inflammation through cytotoxic CD8+ T lymphocytes in patients with FDAF.
  • To explore the role of the TF-factor Xa-factor IIa axis in thrombo-inflammation and its link to PAR1 and CD8+ T cells in AF.

Main Methods:

  • Analysis of data and blood samples from 210 patients, including 160 with FDAF, 32 with paroxysmal AF, and 20 controls.
  • Assessment of circulating CD8+ T lymphocyte subsets and plasma levels of CD8+ effector molecules.
  • Evaluation of tissue factor (TF) and PAR1 activation in relation to inflammatory and cytotoxic functions and MACE occurrence.

Main Results:

  • Early AF showed increased pro-inflammatory and cytotoxic CD8+ T lymphocytes compared to controls, with elevated effector molecules correlating with cardiac remodeling and atrial dysfunction biomarkers.
  • Activation of TF and PAR1 was associated with pro-inflammatory and cytotoxic CD8+ T cell functions.
  • PAR1-mediated CD8+ T cell activation was more prevalent in FDAF patients who experienced MACE.

Conclusions:

  • The TF-factor Xa-factor IIa cascade contributes to thrombo-inflammation via PAR1 in CD8+ T cells in FDAF patients.
  • Targeting this thrombo-inflammatory cascade presents a potential synergistic strategy to mitigate AF progression and vascular complications.
Abstract

Keywords:
CD8MACEPAR1atrial fibrillationatrial myopathyprotease-activated receptort cellsthrombinthrombo-inflammationtissue factor

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