A new German study published in Brain, Behavior, and Immunity by Loebel, et al. has found that Chronic Fatigue Syndrome* may be an infection-triggered autoimmune disease, at least in a subset of patients studied.
Samples from a large cohort (n=268) in Berlin and a smaller sample of patients treated with Rituximab (n=25) were measured against controls (n=168). Researchers found that antibodies against a neurotransmitter receptor were elevated in 29.5% of patients. Specifically, antibodies to ß2 adrenergic and M3 and M4 muscarinic cholinergic receptors, which are both G protein-coupled receptors (GCPRs).
Serum IgG against GCPRs were measured using an ELISA test.
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.
This work extends previous research by Fluge, et al. which showed that 60% of CFS patients in their study achieved partial or full remission on Rituximab, which depletes CD20+ B cells, a component of the immune system. There are many different types of B cells. That it took five months for patients to see effects suggested to these researchers that it wasn’t directly the depletion of B cells causing the clinical effect, but rather the wiping out of memory B cells and the autoantibodies they were presumed to be creating against some unidentified target. With this new paper, Loebel, et al. believe they may have found that target.
Recent studies have found autoantibodies to ß1 and ß2 adrenergic receptors in Postural Orthostatic Tachycardia (POTS). ß adrenergic and muscarinic autoantibodies have been described in other autoimmune and neurological diseases. In addition to POTS, ß adrenergic autoantibodies have been found in orthostatic hypotension, dialated cardiomyopathy and Chagas disease, Muscarinic autoantibodies have been found in Myasthenia gravis, Sjorgen’s and schizophrenia. Both have been found in Graves’ disease.
The authors note that their finding of autoantibodies to ß2, M3, and M4 receptors does not exclude that additional autoantibodies not included in this study could also be at play.
*The term Chronic Fatigue Syndrome is used here as that is the term the study’s authors use. Patients were selected using the Canadian Consensus Criteria.
#MEAction Gives Thanks
November 27, 2024
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We have come to the time of year, where we focus on what we are thankful for and what has made a difference in our lives. At #MEAction we will always be thankful for this amazing community, for you truly are OUT OF THIS WORLD! With this focus, #MEAction staff share what they are most
5 thoughts on “Autoantibodies found in subset of CFS patients”
Wondered for some time if we have something like Anti-NMDA Receptor Autoimmune Encephalitis, but with different receptors. Maybe this work supports that for at least some patients? However, what do the other patients have? Maybe we are really a mix of different autoimmune conditions, lumped together by symptomology?
I have Hypotension but it was never called Orthostatic Hypotension. I fainted during a table tilt test 20 or so years ago but never got a diagnosis then; Hypotension was diagnosed a few years ago and I went on Fludrocortisone.
I was a functioning undiagnosed patient from 18 to 38 and then I left my job and then a few years later trying to work completely imploded and became disabled by 42. Doctors were throwing depression meds at me, Cymbalta for my Fibro, it all went wrong. Now, even my dermatologist knows Fibro and ME/CFS are autoimmune and won’t give me a medication he knows that any hormone will cause more problems. Too late, a couple years earlier my OBGYN insisted I take a hormone for hot flashes and it was a disaster.
I am faxing the PUBMED summary to all my doctors.
I became ill after being diagnosed with cmv related to ebv. Even after virus titers returned to normal I continued with chronic fatigue flares, and other symptoms. In 1991 I slipped on ice and cement and became disabled with CFS,FM, Sjrogens disease, and Hypotension. I was put on amitriptyline but as dosage increased so did my weight and brain fog. Doctor changed meds to other antidepressants, which gave me horrible side effects. Then she tried tramadol and sleep meds, but continued with bad fatigue and pain,ibs, etc. Then Savella was the new cfs/fm drug. But the doctor still had me on tramadol, which combined with the Savella sent me into Serotonin syndrome. A living nightmare!! Doctor didn’t want to treat me anymore. Found a rheumatologist and he was using a drug called NUCYNTA for patients with post traumatic fibromyalgia. This drug with small doses of tramadol and sleep med, low dose Ritalin and atenonol, helped me get out occasionally and attend my son’s wedding 2 yrs ago. However NUCYNTA and tramadol are no longer available since last year when Massachusetts stopped prescribing anything with pain medication unless you had cancer, because some people abuse medications. Slowly I have returned to bedridden or homebound, going on 28 years. I would love the opportunity to try rituximab treatment, I’ve watched my life pass by and have suffered so much loss. I’m going to be 67 years old soon. It would also give my son who,s wedding I attended, a chance of a better life than me as he,s now ill with Me/cfids. How long before we can try this new medication US.
Finally figured out CFS is an infection huh
Dr. William Baumzweiger, a most courageous, former VA Doctor, had stated over a dozen years ago – SO THEY DO KNOW (yet the VA canned him for giving “non-approved” IV Drips, which DO temporarily help those who are chronically LOW in BLOOD VOLUME & BLOOD PRESSURE) – but they’re only a problematic Band-Aid – as it can tip a PWC into HIGH BV & BP – as it did me & as I reported in the October 2000 only SOS Conference – which was ‘fixed’ ) – that this IS “BRAINSTEM ENCEPHALOPATHY”!!!!! Plus I believe I’m probably the only CFS Patient who’s had over 50 (yes – FIFTY +) RITUXIMAB Treatments, and incredibly some of the symptoms seem to have been temporarily mitigated. I’m not ‘fixed’ by any means, however I’ve a glimpse of some former faculties – having lost 51-70 points in my IQ via CFS from back in June 1991. But I also had other Treatments (anti-viral & anti-bacterial) prior. However, the massive Steroids that are required for Rituximab Treatments are majorly problematic, and caused major havoc with my Immune Function & created Proximal Muscle Weakness. DYSREGULATION is my “lay person’s” summary description of this DD. We NEED immediate CLINICAL TRIALS in the US – they OWE us & the multiple millions of PWC / GWS / FM / Asperger’s / Autistic folks to STOP THE TRAGEDY of this DD being PROGRESSIVE & FATAL!!!!! Thus 2016 should be a VERY INTERESTING ELECTION YEAR HERE, because ‘you know who’ certainly KNOWS!”!
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