Reza Mobini
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Reza Mobini has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
Finn Waagstein
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, SE-413 45, Göteborg, Sweden
3 shared publicationsGert Wallukat
Max-Delbrück Center for Molecular Medicine, Berlin-Buch, Germany
2 shared publicationsHans Maschke
BioScience New Business Consulting, Wunstorf, Germany
2 shared publicationsAlexander Staudt
1 shared publicationGert Baumann
Charite
1 shared publicationHelen Svensson
Cardiovascular Institute of the South
1 shared publication
Latest Publications
- 1 September 2004
- Published by Taylor & Francis in Autoimmunity
- Vol. 37 (6-7) , 489-493
Beneficial Effect on Cardiac Function by Intravenous Immunoglobulin Treatment in Patients with Dilated Cardiomyopathy is not due to Neutralization of Anti-receptor Autoantibody
Anti-β1-adrenoceptor (β1AR) autoantibodies have been shown to be pathophysiologically important in idiopathic dilated cardiomyopathy (DCM). Treatment with intravenous immunoglobulin (IVIG) has shown beneficial effects in both DCM and ischemic cardiomyopathy. However, the underlying mechanism has not been clarified. In the present study, we therefore examined whether the improvement of cardiac function was due to neutralization of functional β1AR autoantibodies by anti-idiotypic antibodies. Autoantibodies against the β1AR was analysed in sera from patients with DCM (n=16) and coronary artery disease (CAD) (n=21) treated with IVIG or placebo before, 6 and 12 months. Six month after treatment, DCM patients showed increase in β1AR autoantibodies, mostly in IgG1 and IgG2, whereas in CAD patients mostly in IgG2. No changes in β1AR autoantibodies after 12 months were detected. In summary, our results indicate that improvement of cardiac function by IVIG is not due to neutralization of β1AR autoantibodies.
- 1 September 2004
- Published by Taylor & Francis in Autoimmunity
- Vol. 37 (6-7) , 489-493
Beneficial Effect on Cardiac Function by Intravenous Immunoglobulin Treatment in Patients with Dilated Cardiomyopathy is not due to Neutralization of Anti-receptor Autoantibody
Anti-β1-adrenoceptor (β1AR) autoantibodies have been shown to be pathophysiologically important in idiopathic dilated cardiomyopathy (DCM). Treatment with intravenous immunoglobulin (IVIG) has shown beneficial effects in both DCM and ischemic cardiomyopathy. However, the underlying mechanism has not been clarified. In the present study, we therefore examined whether the improvement of cardiac function was due to neutralization of functional β1AR autoantibodies by anti-idiotypic antibodies. Autoantibodies against the β1AR was analysed in sera from patients with DCM (n=16) and coronary artery disease (CAD) (n=21) treated with IVIG or placebo before, 6 and 12 months. Six month after treatment, DCM patients showed increase in β1AR autoantibodies, mostly in IgG1 and IgG2, whereas in CAD patients mostly in IgG2. No changes in β1AR autoantibodies after 12 months were detected. In summary, our results indicate that improvement of cardiac function by IVIG is not due to neutralization of β1AR autoantibodies.
- 30 June 2004
- Published by Elsevier in Autoimmunity Reviews
- Vol. 3 (4) , 277-284
New insights into the pathogenesis of dilated cardiomyopathy: possible underlying autoimmune mechanisms and therapy
- 30 June 2004
- Published by Elsevier in Autoimmunity Reviews
- Vol. 3 (4) , 277-284
New insights into the pathogenesis of dilated cardiomyopathy: possible underlying autoimmune mechanisms and therapy
- 1 June 2003
- Published by Elsevier in Journal of Autoimmunity
- Vol. 20 (4) , 345-350
Hemodynamic improvement and removal of autoantibodies against β1-adrenergic receptor by immunoadsorption therapy in dilated cardiomyopathy
- 1 June 2003
- Published by Elsevier in Journal of Autoimmunity
- Vol. 20 (4) , 345-350
Hemodynamic improvement and removal of autoantibodies against β1-adrenergic receptor by immunoadsorption therapy in dilated cardiomyopathy