Immunoadsorption to remove ß2 adrenergic receptor antibodies in Chronic Fatigue Syndrome CFS/ME

• Published in: PloS one Vol. 13; no. 3; p. e0193672
• Main Authors: Scheibenbogen, Carmen, Loebel, Madlen, Freitag, Helma, Krueger, Anne, Bauer, Sandra, Antelmann, Michaela, Doehner, Wolfram, Scherbakov, Nadja, Heidecke, Harald, Reinke, Petra, Volk, Hans-Dieter, Grabowski, Patricia
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 15.03.2018; Public Library of Science (PLoS)
• Subjects: Acetylcholine receptors (muscarinic); Adrenergic beta receptors; Adrenergic receptors; Anemia; Antibodies; Autoantibodies; Autoimmune diseases; Autonomic nervous system; Biology and Life Sciences; Cardiomyopathy; Care and treatment; Chronic fatigue syndrome; Chronic illnesses; Chronic infection; Cytometry; Development and progression; Disease; Encephalomyelitis; Enzyme-linked immunosorbent assay; Fatigue; Flow cytometry; Guillain-Barre syndrome; Health aspects; Immunoadsorption; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Immunoglobulins; Immunological memory; Immunology; Infections; Lymphocytes B; Medicine and Health Sciences; Memory cells; Metabolism; Nephrology; Neurotransmitter receptors; Patients; Phenotypes; Phenotyping; Plasma; Plasma cells; Receptors; Receptors (physiology); Research and Analysis Methods; Stroke; United States > US; Germany
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0193672

Infection-triggered disease onset, chronic immune activation and autonomic dysregulation in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) point to an autoimmune disease directed against neurotransmitter receptors. We had observed elevated autoantibodies against ß2 adrenergic receptors, and muscarinic 3 and 4 acetylcholine receptors in a subset of patients. Immunoadsorption (IA) was shown to be effective in removing autoantibodies and improve outcome in various autoimmune diseases. 10 patients with post-infectious CFS/ME and elevated ß2 autoantibodies were treated with IA with an IgG-binding column for 5 days. We assessed severity of symptoms as outcome parameter by disease specific scores. Antibodies were determined by ELISA and B cell phenotype by flow cytometry. IgG levels dropped to median 0.73 g/l (normal 7-16 g/l) after the 4th cycle of IA, while IgA and IgM levels remained unchanged. Similarly, elevated ß2 IgG antibodies rapidly decreased during IA in 9 of 10 patients. Also 6 months later ß2 autoantibodies were significantly lower compared to pretreatment. Frequency of memory B cells significantly decreased and frequency of plasma cells increased after the 4th IA cycle. A rapid improvement of symptoms was reported by 7 patients during the IA. 3 of these patients had long lasting moderate to marked improvement for 6-12+ months, 2 patients had short improvement only and 2 patients improved for several months following initial worsening. IA can remove autoantibodies against ß2 adrenergic receptor and lead to clinical improvement. B cell phenotyping provides evidence for an effect of IA on memory B cell development. Data from our pilot trial warrants further studies in CFS/ME.