Autoimmunität
Tóm tắt
Die immunologische Toleranz gegenüber Selbstantigenen wird durch zwei Mechanismen gewährleistet, nämlich der Deletion von potenziell selbstreaktiven T-Lymphozyten im Thymus („negative Selektion“) sowie der aktiven Suppression von unerwünschten (Auto)Immunreaktionen im peripheren Immunsystem durch regulatorische T-Zellen (Treg). Mit wenigen Ausnahmen entstehen Autoimmunerkrankungen durch eine multifaktoriell bedingte Störung der Homöostase des Immunsystems. Dabei spielen neben einer genetischen Prädisposition auch eine unerwünschte Aktivierung des Immunsystems durch exogene (z. B. Infektionen) oder endogene Stimuli (z. B. gestörte Barrierefunktion) eine Rolle. Toll-like-Rezeptorliganden von mikrobiellen Erregern können mit der Aktivierung von Immunzellen auf mehreren Ebenen interferieren: Stimulierung von autoreaktiven B-Lymphozyten, Verstärkung von Autoantigenpräsentation gegenüber T-Lymphozyten oder auch Modulation der Suppressorfunktion von Treg. Für die Entzündungsreaktion und die damit verbundene Gewebezerstörung bei Autoimmunerkrankungen spielen darüber hinaus die erst kürzlich entdeckten Interleukin 17 produzierenden Th17-T-Lymphozyten eine besondere Rolle.
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