Publikationen
HSA als Mitautor
HSA beteiligt sich an der wissenschaftlichen Gemeinschaft sowohl als Mitautor von Veröffentlichungen als auch als Werkzeug für die Forschung. Hier finden Sie eine Auswahl unserer Publikationen und der Arbeiten, an denen HSA beteiligt war.
Abstract
Modules Used
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Modules Used
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Abstract
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Abstract
Deregulated complement activation contributes to or drives the pathogenesis of various kidney diseases. Targeting complement is a therapeutic option.1,2Inhibition on the level of C5 is an established therapy in atypical hemolytic uremic syndrome (aHUS), paroxysmal nocturnal hemoglobinuria, and myasthenia gravis, and novel drugs targeting other components of the complement cascade are being developed.3,4Currently, the diagnosis of complement activation in kidney diseases is based primarily on immunohistochemical detection of deposited complement activation products in tissue and the detection of consumption of complement components in plasma.5
To date, a method to directly identify, localize, quantify, and differentiate complement convertases in tissue has been lacking. We therefore established an in situ method to detect and localize assembled C3/C5 convertases of the classical/lectin and alternative pathways (Figure 1;Supplementary Methods;Supplementary Figures S1–S4). We utilized a bright field proximity ligation assay6,7because (i) the microanatomic context is preserved, allowing, for example, selection of preserved glomeruli and the exact localization of the signals, and (ii) the signals are stable and easily quantifiable. Close proximity of C2 and C4b was used to identify assembled classical/lectin C3/C5 convertases, and of C3b and Bb, the fragment of factor B, to identify the alternative C3/C5 convertase.