Wechselwirkungen zwischen Gefäßendothel und Leukozyten

Zusammenfassung

Granulozyten, Monozyten und Lymphozyten können ihre Aufgabe im Rahmen der Erkennung von körperfremden Antigenen und der Abwehr von Mikroorganismen nur erfüllen, wenn sie aus dem intravasalen Raum nach extravasal emigrieren. Dies erfordert ihre Adhäsion an die Gefäßwand und aktive Permeation der Endothelbarriere. Unter physiologischen Bedingungen kommt es hierbei bereits zu vielseitigen Wechselwirkungen zwischen Leukozyten und dem Gefäßendothel, bei denen eine Reihe von Mediatoren beteiligt sind (Interleukine, Monokine, chemotaktische Faktoren, Wachstumsfaktoren etc.).

Bei der Interaktion von Granulozyten und Monozyten mit der Gefäßwand befindet sich das Endothel weitgehend in einer passiven Rolle. Gegenüber Lymphozyten dagegen übernimmt das Endothel auch wichtige Effektorfunktionen. So aktivieren Endothelzellen T-Lymphozyten durch Antigenpräsentation und Interleukin- 1-Freisetzung. Umgekehrt versetzen T-Lymphozyten Endothelzellen durch Induktion von Klasse-II-Transplanta- tionsantigenen erst in die Lage, mit T-Lymphozyten zu kooperieren.

In der Pathogenese vieler Entzündungsreaktionen, aber auch Erkrankungen wie der Schocklunge können diese immunpathogenetischen Vorgänge zu einer Endothelläsion und damit Zerstörung der Endothelschranke führen. Hierbei kann je nach Krankheitsbild die Interaktion mit Granulozyten, Lymphozyten und/ oder Endothel-spezifischen Antikörpern bzw. Komplement im Vordergrund stehen.

Monozyten setzen potente Mediatoren frei (Monokine, Lymphokine), die eine Wirkung auf Endothel, aber auch glatte Muskelzellen der Gefäßwand haben. Von großem Interesse ist hierbei insbesondere die Rolle der Monozyten in der Pathogenese der Atherosklerose.

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