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<p>Inflammatory processes in and on the vascular wall are characterized by the interplay of platelets with various immune cells, including monocytes, neutrophil granulocytes, T&#xa0;and&#xa0;B cells. In this context, signaling proteins, such as cytokines and chemokines as well as nucleotides and microvesicles play a&#xa0;critical role. However, direct physical interactions via surface receptors also result in the formation of platelet-leukocyte aggregates. A&#xa0;key factor in this process is the association of P‑selectin (CD62P) on the surface of platelets with P‑selectin glycoprotein ligand‑1 (PSGL-1) on immune cells. This type of interaction mostly results in a&#xa0;bidirectional activation and leads to increased release of cytokines, chemokines and coagulation factors. While this mechanism supports the immune response against pathogens, it can also exacerbate tissue damage in sterile or autoinflammatory inflammation. Elevated levels of monocyte-platelet or neutrophil-platelet aggregates are observed in a&#xa0;range of inflammatory diseases, with evidence suggesting a&#xa0;correlation between the abundance of these complexes and disease severity or progression. For this reason, platelet-leukocyte aggregates are discussed as potential biomarkers. Although it is assumed that these complexes have a high relevance in the pathophysiology of vascular inflammation, the precise mechanisms remain incompletely understood. This review article summarizes the current knowledge on the key principles and mechanisms underlying platelet-leukocyte aggregate formation and explores their role in inflammatory diseases of the vascular system.</p>

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Die Rolle von Plättchen-Leukozyten-Komplexen bei entzündlichen Erkrankungen des Gefäßsystems

  • 期刊论文

  • 发表日期：

    2025年1月10日

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  • Lisa-Marie Irschfeld,
  • Patricia Kleimann,
  • Zeynep-Büsra Tiren,
  • Talia Ahrazoglu,
  • Jennifer Isabel Kluczny,
  • Florian Simon,
  • Sebastian Temme

摘要

Inflammatory processes in and on the vascular wall are characterized by the interplay of platelets with various immune cells, including monocytes, neutrophil granulocytes, T and B cells. In this context, signaling proteins, such as cytokines and chemokines as well as nucleotides and microvesicles play a critical role. However, direct physical interactions via surface receptors also result in the formation of platelet-leukocyte aggregates. A key factor in this process is the association of P‑selectin (CD62P) on the surface of platelets with P‑selectin glycoprotein ligand‑1 (PSGL-1) on immune cells. This type of interaction mostly results in a bidirectional activation and leads to increased release of cytokines, chemokines and coagulation factors. While this mechanism supports the immune response against pathogens, it can also exacerbate tissue damage in sterile or autoinflammatory inflammation. Elevated levels of monocyte-platelet or neutrophil-platelet aggregates are observed in a range of inflammatory diseases, with evidence suggesting a correlation between the abundance of these complexes and disease severity or progression. For this reason, platelet-leukocyte aggregates are discussed as potential biomarkers. Although it is assumed that these complexes have a high relevance in the pathophysiology of vascular inflammation, the precise mechanisms remain incompletely understood. This review article summarizes the current knowledge on the key principles and mechanisms underlying platelet-leukocyte aggregate formation and explores their role in inflammatory diseases of the vascular system.