Antibodies to ß adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syn

sue la-la

Member
http://www.ncbi.nlm.nih.gov/pubmed/26399744
Brain Behav Immun. 2015 Sep 20. pii: S0889-1591(15)30020-9. doi: 10.1016/j.bbi.2015.09.013. [Epub ahead of print]

Antibodies to ß adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syndrome.

Loebel M1, Grabowski P2, Heidecke H3, Bauer S2, Hanitsch LG2, Wittke K2, Meisel C4, Reinke P5, Volk HD6, Fluge Ø7, Mella O8, Scheibenbogen C6.
Author information

Abstract

Infection-triggered disease onset, chronic immune activation and autonomic dysregulation in CFS point to an autoimmune disease directed against neurotransmitter receptors. Autoantibodies against G-protein coupled receptors were shown to play a pathogenic role in several autoimmune diseases. Here, serum samples from a patient cohort from Berlin (n= 268) and from Bergen with pre- and post-treatment samples from 25 patients treated within the KTS-2 rituximab trial were analysed for IgG against human α and ß adrenergic, muscarinic (M) 1-5 acetylcholine, dopamine, serotonin, angiotensin, and endothelin receptors by ELISA and compared to a healthy control cohort (n=108). Antibodies against ß2, M3 and M4 receptors were significantly elevated in CFS patients compared to controls. In contrast, levels of antibodies against α adrenergic, dopamine, serotonin, angiotensin, and endothelin receptors were not different between patients and controls. A high correlation was found between levels of autoantibodies and elevated IgG1-3 subclasses, but not with IgG4. Further patients with high ß2 antibodies had significantly more frequently activated HLA-DR+ T cells and more frequently thyreoperoxidase and anti-nuclear antibodies. In patients receiving rituximab maintenance treatment achieving prolonged B-cell depletion, elevated ß2 and M4 receptor autoantibodies significantly declined in clinical responder, but not in non-responder. We provide evidence that 29.5% of patients with CFS had elevated antibodies against one or more M acetylcholine and ß adrenergic receptors which are potential biomarkers for response to B-cell depleting therapy. The association of autoantibodies with immune markers suggests that they activate B and T cells expressing ß adrenergic and M acetylcholine receptors. Dysregulation of acetylcholine and adrenergic signalling could also explain various clinical symptoms of CFS.

Copyright © 2015. Published by Elsevier Inc.
PMID: 26399744
[PubMed - as supplied by publisher]
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Potentially huge paper!

Have they found the Rituximab subset? They've been looking for autoantibodies for years....

VERY BIG...:) Definitely will do a blog on this one.

In patients receiving Rituximab, those who were responders had significantly lower levels of ß2 and M4 autoantibodies after treatment. The authors suggest that these autoantibodies could be biomarkers to those CFS patients most likely to respond to Rituximab treatment.
 

etherspin

New Member
looking forward to the blog post because I could only parse enough text to know this was very promising, but not why it was so ! :)
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
looking forward to the blog post because I could only parse enough text to know this was very promising, but not why it was so ! :)
I'm looking forward to figuring that out too. It appears they have evidence of autoimmunity in a subset of ME/CFS patients and those are th patients that respond to Rituximab. If they do you could get tested for the autoantibodies and if you were positive you would probably respond to Rituximab!

If all that is true, this finding would ultimately break up this disease.....A new autoimmune disease would have been found and then there would be the rest of us.

I'm hoping that's right :cool: I 'm trying to get the paper.
 

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