Pathogenese der Uveitis

Uveitis, an inflammation of the inner eye, can have various causes: autoimmunity is the most common in Europe, while trauma, infection, or masquerade syndromes are less common. This article summarizes the current knowledge on the pathogenesis of autoimmune uveitis. The immune privilege of the eye prevents the local activation of the immune system; instead, it is postulated that there is extraocular activation with environmental antigens resembling ocular protein (antigenic mimicry), which are then mistaken for ocular autoantigens by T cells. The T cells recruit the inflammatory cells responsible for tissue destruction into the eye. T helper (Th)-1 and Th17 cells that recognize ocular autoantigens play a major role in uveitis; these can also differentiate in the eye into Th1/Th17 mixed types or even into regulatory cells. There are genetic associations with various types of uveitis, most notably with HLA class I molecules. However, numerous other genes that influence the immune response have also been found. The microbiome, which plays an instrumental role as a “training partner” for cells of the immune system, is also discussed as a possible trigger for uveitis, either through antigenic mimicry of bacterial molecules similar to ocular autoantigens or by causing an imbalance of the immune system.