Publikationsserver der Universitätsbibliothek Marburg
Titel:Einfluss einer gain-of-function-Mutation im Plcg2-Gen auf eine Helicobacter felis-induzierte gastrale MALT-Lymphom Entwicklung
Autor:Goßmann, Jennifer
Weitere Beteiligte: Neubauer, Andreas (Prof. Dr.)
Veröffentlicht:2015
URI:https://archiv.ub.uni-marburg.de/diss/z2016/0003
URN: urn:nbn:de:hebis:04-z2016-00030
DOI: https://doi.org/10.17192/z2016.0003
DDC: Medizin
Titel (trans.):A gain-of-function mutation in the Plcg2 gene protects mice from Helicobacter felis-induced gastric MALT lymphoma
Publikationsdatum:2016-01-25
Lizenz:https://creativecommons.org/licenses/by-nc-sa/4.0

Dokument

Schlagwörter:
Phospholipase C gamma 2, Helicobacter, gastrales MALT-Lymphom, Helicobacter, Phospholipase C gamma 2, gastric MALT lymphoma, regulatorische T-Zellen, regulatory T-cells

Zusammenfassung:
Das Marginalzonen B-Zell-Lymphom vom MALT (mucosa-associated lymphoid tissue)-Typ des Magens ist eine Modellerkrankung für das Verständnis, wie eine bösartige Tumorerkrankung aus einer chronischen bakteriellen Helicobacter pylori-Infektion entstehen kann. Unsere Arbeitsgruppe war eine der Ersten die zeigen konnte, dass eine Eliminierung von H. pylori im frühen Stadium eines MALT-Lymphoms in vielen Fällen eine langanhaltende Remission bewirkt. Eine H. pylori-Eradikation stellt somit die Therapie erster Wahl im frühen Stadium eines gastralen MALT-Lymphoms dar. Neben Helicobacter-spezifischen Virulenzfaktoren spielen spezifische Wirtsmerkmale bei der Entwicklung von MALT-Lymphomen eine ganz entscheidende Rolle. So führen verschiedene Wirtsgen-Polymorphismen, die für die Immunantwort und Entzündungsreaktion einer H. pylori-Infektion verantwortlich sind, zu einer gesteigerten inflammatorischen Antwort und zu einer stärkeren Neigung, gastrale MALT-Lymphome zu entwickeln. Zudem konnte unsere eigene Arbeitsgruppe zeigen, dass das Gen Phospholipase C gamma 2 in gastralen MALT-Lymphomen, im Vergleich zur chronischen Entzündungsreaktion, überexprimiert ist. Vor diesem Hintergrund untersucht die vorliegende Arbeit, inwieweit Mäuse, die aufgrund einer gain-of-function-Mutation im Plcg2-Gen Symptome einer gesteigerten Entzündungsreaktion und Autoimmunerkrankungen zeigen, eine frühere und höhere Inzidenz aufweisen, H. felis-induzierte MALT-Lymphome zu entwickeln. Eine H. felis-Infektion in Mäusen ruft dabei ganz ähnliche Symptome hervor wie eine humane H. pylori-Infektion. Entgegen der Erwartung konnte gezeigt werden, dass heterozygote Plcg2Ali5/+ Mäuse, im Vergleich zu WT Mäusen, signifikant weniger gastrale MALT-Lymphome entwickeln. Dies wurde von einer Herunterregulation proinflammatorischer Gene und einer verringerten H. felis-spezifischen Antikörperantwort in Plcg2Ali5/+ Mäusen begleitet. Ein B-Zell-Defekt in Plcg2Ali5/+ Mäusen konnte durch in vitro Experimente ausgeschlossen werden. Die Untersuchung regulatorischer T-Zellen im Milzgewebe beider Genotypen zeigte, dass Plcg2Ali5/+ Mäuse eine signifikant höhere Anzahl immunsuppressiver CD73 exprimierender Tregs besitzen. Anhand dieses Ergebnisses lässt sich die in Plcg2Ali5/+ Mäusen verringerte Immunantwort gegenüber einer Helicobacter-Infektion erklären. In dieser Arbeit konnte somit erstmals gezeigt werden, dass die gain-of-function-Mutation im Plcg2-Gen vor einer Helicobacter-induzierten MALT-Lymphom Entwicklung schützt. Die Experimente und Auswertungen innerhalb dieser Arbeit lassen die Schlussfolgerung zu, dass die in Plcg2Ali5/+ Mäusen auftretende erhöhte Anzahl von Tregs möglicherweise für die geringere Entzündungsreaktion und folglich für die reduzierte Entstehung des Lymphoms verantwortlich ist.

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