G-protein coupled receptor auto-antibodies in thromboangiitis obliterans (Buerger’s disease) and their removal by immunoadsorption

Author:

Klein-Weigel Peter F.1,Bimmler Marion2,Hempel Petra2,Schöpp Sebastian3,Dreusicke Siegrid1,Valerius Jana1,Bohlen Anne1,Boehnlein Joana M.1,Bestler Daniel4,Funk Stephanie3,Elitok Saban3

Affiliation:

1. HELIOS Klinikum Berlin-Buch, Klinik für Angiologie, Germany

2. E.R.D.E.-AKK-Diagnostik GmbH, Berlin, Germany

3. Klinik für Kardiologie und Nephrologie, HELIOS Klinikum Berlin-Buch, Germany

4. Klinik für Allgemeine Innere Medizin und Gastroenterologie, HELIOS Klinikum Berlin-Buch, Germany

Abstract

Background: Immunhistopathological and serological data favors an immunopathogenesis of thromboangiitis onliterans(TAO, Buerger’s disease). Autoantbodies seem to play a major role. Immunoadsorption (IA) proved to be therapeutically effective. We focused on agonistic autoantibodies (agAAB) directed against G-protein coupled receptors (GPCR) and proved the hypothesis, that these agAAB might be present in TAO and that a five day course of IA might be able to eliminate these agAAB effectively. Patients and methods: Between December 2012 and May 2014 11 TAO-patients were treated by IA in a five day course. AgAAB-analysis was performed using specific ELISA techniques. Results: AgAAB were detected in 9 out of 11 patients (81.8 %).Multiple agAAB were present in 7 patients (63.6 %). A clustering of agAAB directed against loop1 of the adrenergic α1-receptor and the endothelin-A-(ETA)receptor was identified, representing 72.7 % resp. 54.5 % of the patients. AgAAB directed against the angiotensin-1 (AT-1) epitope 1 or 2 were detected in 3 patients and agAAB directed against protease-activated receptor (PAR) loop1/2 were seen in 2 patients. AgAAB directed against ETA-receptor loop1 never appeared without agAAB directed against α1-receptor loop1. Immediately after a five day-course of IA agAAB were absent in 81.8 % of the total study group and in 77.8 % of all cases tested positive for agAAB before IA. Conclusions: AgAAB directed against GPCR were identified in TAO patients with a clustering of agAAB directed against α-1-adrenergic receptor loop1 and ETA-receptor loop1. AgAA were eliminated by IA in the majority of cases. We suggest that these agAA play an important role in the pathogenesis of TAO and that their elimination might be responsible for the positive therapeutic effects reported in patients treated with IA.

Publisher

Hogrefe Publishing Group

Subject

Cardiology and Cardiovascular Medicine

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