Angeborene Immunität und Infektionen durch bekapselte Bakterien

Zusammenfassung

Invasive Infektionen durch Meningokokken und Pneumokokken sind wichtige Ursachen für Morbidität und Letalität im Säuglings- und Kleinkindalter. Der klinische Verlauf variiert von relativ milden klinischen Manifestationen bis hin zu fulminantem septischem Schock mit einer Letalität bis zu 90 %. Immunologische Mechanismen, die von Geburt an aktiv sind (das sog. Angeborene Immunsystem), spielen eine wichtige Rolle bei der Abwehr gegenüber invasiven Meningokokken- und Pneumokokken-Infektionen, insbesondere im „vulnerablen Fenster” nach dem Abfall der mütterlich erworbenen Antikörper (Nestschutz) und vor der vollständigen Entwicklung adaptiver Immunmechanismen. Es wird zunehmend deutlich, dass Defekte in Schlüsselmolekülen des angeborenen Immunsystems, wie dem Mannose bindenden Lektin (MBL) oder Mitgliedern der Toll-like-Rezeptor-Superfamilie (wie TLR4 und andere), für das Auftreten von Meningokokken- und/oder Pneumokokken-Infektionen disponieren, den klinischen Phänotyp und Verlauf modulieren oder beides. Dieser Effekt erscheint am meisten prävalent in der „vulnerablen Phase” des Säuglingsalters, bevor andere redundante Mechanismen des Immunsystems vollständig ausgereift sind.

Abstract

Meningococcal and pneumococcal diseases are important causes of morbidity and mortality in infancy and childhood. The clinical course ranges from relatively benign clinical manifestations to fulminant septic shock with mortality rate up to 90 %. Immune components, which are constitutively present from birth (the innate immune system) help to protect infants from meningococcal and pneumococcal infection especially in the „vulnerable window” after decline of transplacental acquired maternal antibodies and before full development of adaptive immune mechanisms. Accumulating evidence suggests that genetic defects in key components of the innate immune system such as Mannose binding Lectin or members of the Toll like receptor Superfamily (TLR4 and others) might either predispose for the onset of meningococcal or pneumococcal disease or modulate the clinical phenotype or both. This effect seems to be most predominant in the vulnerable phase of infancy before other redundant immune mechanisms are not yet fully developed.

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