Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation
Jonathan Mandel1, Martina Casari1, Maria Stepanyan1,2,3,4
1Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University, 55131 Mainz, Germany.
Platelets are key immune cells beyond clotting, regulating neutrophils and macrophages in inflammation, infection, and cancer. This review explores platelet receptors and granule secretions in diseases like atherosclerosis, TRALI, and COVID-19.
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- Platelets traditionally known for hemostasis and thrombosis.
- Emerging evidence highlights platelet roles in immunity, inflammation, infection, and cancer.
- Platelets interact with and regulate innate immune cells like neutrophils, monocytes, and macrophages.
Purpose of the Study:
- To review platelet activation in hemostatic and inflammatory processes.
- To examine platelet interactions with neutrophils and monocytes/macrophages.
- To detail the contribution of platelet receptors and granule secretions in various diseases.
Main Methods:
- Literature review focusing on platelet function beyond hemostasis.
- Analysis of major platelet receptors (GPIb, αIIbβ3, TLT-1, CLEC-2, TLRs).
- Examination of platelet granule secretions and their impact on immune cell function.
Main Results:
- Platelet receptors and secretions are crucial for platelet-neutrophil interactions, including aggregate and NET formation.
- These interactions are implicated in atherosclerosis, transfusion-related acute lung injury (TRALI), and COVID-19.
- Platelet-monocyte/macrophage interactions are significant in cancer metastasis, infection, sepsis, and platelet clearance.
Conclusions:
- Platelets are critical regulators of innate immunity and inflammation.
- Platelet receptors and secreted factors mediate complex interactions with immune cells in disease pathogenesis.
- Understanding these interactions offers potential therapeutic targets for inflammatory and infectious diseases.
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