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Hamostaseologie 2018; 38(04): 186-202
DOI: 10.1055/s-0038-1669450
Review Article
Georg Thieme Verlag KG Stuttgart · New York

The Mutual Relation of Platelet Activation and Innate Immunity

Felix Eisinger
1   Section for Cardioimmunology, Department of Cardiovascular Medicine, University of Tuebingen, Tuebingen, Germany
,
Harald F. Langer
1   Section for Cardioimmunology, Department of Cardiovascular Medicine, University of Tuebingen, Tuebingen, Germany
2   University Clinic for Cardiovascular Medicine, University of Tuebingen, Tuebingen, Germany
› Author Affiliations
Further Information

Publication History

17 April 2018

19 July 2018

Publication Date:
25 September 2018 (online)

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Abstract

Platelets are known to be central regulators of haemostasis, inflammation and immune response. Formed by megakaryocytes in the bone marrow and the lungs, platelets express a broad range of adhesion receptors and release cytokines and platelet microparticles which enable them to interact with both immune cells and pathogens. In bacterial and viral infections, thrombophilia and thrombocytopenia are commonly seen symptoms, indicating the close relationship between haemostasis and immune defence. Indeed, platelets contribute both directly and via immune mediation to pathogen clearance. In sterile inflammation, a pathogen-free process which is often triggered by cell necrosis and autoimmune reactions, platelets are also of central importance. Recently, platelet inflammasome has been extensively studied in this context. Both sterile inflammation and infection are affected by the interactions of platelets and innate immunity, notably the complement system. Although the general elements of this interplay have been known for long, more and more insights into disease-specific mechanisms could be gained recently. This review gives an outline of the current findings in the field of platelet–immune cell interactions and points out possible implications for clinical therapy.

Zusammenfassung

Thrombozyten sind bekanntlich zentrale Regulatoren von Blutstillung, Entzündung und Immunantwort. Gebildet von Megakaryozyten im Knochenmark und in der Lunge, exprimieren Plättchen eine breite Palette von Adhäsionsrezeptoren und setzen Cytokine und Plättchenmikropartikel frei, die es ihnen ermöglichen, sowohl mit Immunzellen als auch mit Pathogenen in Wechselwirkung zu treten. Bei bakteriellen und viralen Infektionen treten häufig Thrombophilie und Thrombozytopenie auf, was auf eine enge Beziehung zwischen Hämostase und Immunabwehr hinweist. In der Tat tragen Thrombozyten sowohl direkt als auch über die Immunmediation zur Pathogenclearance bei. Bei der sterilen Entzündung, einem pathogenfreien Prozess, der häufig durch Zellnekrose und Autoimmunreaktionen ausgelöst wird, sind Thrombozyten ebenfalls von zentraler Bedeutung. In letzter Zeit wurde das Thrombozyten-Inflammasom in diesem Zusammenhang ausführlich untersucht. Sowohl sterile Entzündungen als auch Infektionen werden durch die Wechselwirkungen von Blutplättchen und angeborener Immunität, insbesondere des Komplementsystems, beeinflusst. Obwohl die allgemeinen Elemente dieses Zusammenspiels seit langem bekannt sind, konnten in letzter Zeit mehr und mehr Einsichten in krankheitsspezifische Mechanismen gewonnen werden. Dieser Artikel gibt einen Überblick über die aktuellen Ergebnisse auf dem Gebiet der Wechselwirkungen zwischen Blutplättchen und Immunzellen und zeigt mögliche Implikationen für die klinische Therapie auf.

Keywords

platelets - innate immunity - inflammation - infection - cytokines - inflammasome - leukocytes - complement system

Schlüsselwörter

Blutplättchen - angeborene Immunität - Entzündung - Infektion - Zytokine - Inflammasom - Leukozyten - Komplementsystem
 

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