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Tryptophan-immunoadsorption plasmapheresis regulates polymorphonuclear-myeloid-derived suppressor cells and pro-inflammatory cytokines.
Ther Apher Dial
November 2024
Department of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Article Synopsis
- The study explores how immunoadsorption plasmapheresis (IA) affects the levels of myeloid-derived suppressor cells (MDSCs), which may help in managing autoimmune diseases.
- It involved 21 patients with autoimmune neurological conditions and 8 healthy participants, measuring immune cell types and inflammatory markers before and after IA treatment.
- Results showed that IA significantly increased the number of specific MDSCs and reduced clinical symptoms in certain patients, suggesting IA may help mitigate autoimmune responses and tissue damage.
The Utility of Miniaturized Adsorbers in Exploring the Cellular and Molecular Effects of Blood Purification: A Pilot Study with a Focus on Immunoadsorption in Multiple Sclerosis.
Int J Mol Sci
February 2024
Division of Neuroimmunology, Department of Neurology, Rostock University Medical Center, 18147 Rostock, Germany.
Immunoadsorption (IA) has proven to be clinically effective in the treatment of steroid-refractory multiple sclerosis (MS) relapses, but its mechanism of action remains unclear. We used miniaturized adsorber devices with a tryptophan-immobilized polyvinyl alcohol (PVA) gel sorbent to mimic the IA treatment of patients with MS in vitro. The plasma was screened before and after adsorption with regard to disease-specific mediators, and the effect of the IA treatment on the migration of neutrophils and the integrity of the endothelial cell barrier was tested in cell-based models.
View Article and Find Full Text PDFChimeric AQP4-based immunosorbent for highly-specific removal of AQP4-IgG from blood.
J Chromatogr A
February 2024
MOE Key Laboratory of Bio-Intelligent Manufacturing, School of Bioengineering, Dalian University of Technology, Dalian, Liaoning 116023, China; Liaoning Key Laboratory of Molecular Recognition and Imaging, School of Bioengineering, Dalian University of Technology, Dalian, Liaoning 116023, China. Electronic address:
Anti-aquaporin-4 autoantibodies (AQP4-IgG) are implicated in the pathogenesis of neuromyelitis optica spectrum disorders (NMOSD), and their removal from the blood circulation is considered to be an effective method for acute treatment. An ideal extracorporeal AQP4-IgG removal system should have high specificity, which means that it can selectively remove AQP4-IgG without affecting normal immunoglobulins. However, the conventional tryptophan immobilized column lacks sufficient specificity and cannot achieve this goal.
View Article and Find Full Text PDFImmunoadsorption as maintenance therapy for refractory neuromyelitis optica spectrum disorder.
Ther Adv Neurol Disord
February 2023
Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke gGmbH, Milchberg 21, 82335 Berg, Germany.
Background: Neuromyelitis optica spectrum disorder (NMOSD) is a rare relapsing autoimmune disease of the central nervous system, affecting mainly optic nerves and spinal cord. NMOSD pathophysiology is associated with anti-aquaporin-4 (AQP4) immunoglobulin G (IgG) autoantibodies. Rapid extracorporeal elimination of autoantibodies with apheresis techniques, such as immunoadsorption (IA), was proven to be an effective treatment of NMOSD attacks.
View Article and Find Full Text PDFImmunoadsorption therapy in refractory heart failure patients with dilated cardiomyopathy: a potential therapeutic option.
Rev Assoc Med Bras (1992)
February 2023
Eskisehir Osmangazi University, Hematology Department - Eskişehir, Turkey.
Objective: Removal of cardiac autoantibodies by immunoadsorption might confer clinical improvement in dilated cardiomyopathy. In this pilot study, we investigated the efficacy and safety of immunoadsorption therapy in refractory heart failure patients with dilated cardiomyopathy.
Methods: This study consisted of 9 heart failure patients with dilated cardiomyopathy, NYHA III-IV, left ventricular ejection fraction <30%, unresponsive to heart failure therapy, and with cardiac autoantibodies.
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