Autoimmune hypothesis: Difference between revisions

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Autoimmune disease is one of several illnesses or conditions experienced alongside of [[ME/CFS]].<ref>{{Cite web|url=https://ammes.org/overlapping-conditions/|title=Overlapping Conditions – American ME and CFS Society|website=ammes.org|language=en-US|access-date=2018-08-12}}</ref>
Autoimmune disease is one of several illnesses or conditions experienced alongside of [[ME/CFS]].<ref>{{Cite web|url=https://ammes.org/overlapping-conditions/|title=Overlapping Conditions – American ME and CFS Society|website=ammes.org|language=en-US|access-date=2018-08-12}}</ref>


Samples from a large cohort (n=268) in Berlin, Germany 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 receptor|adrenergic]] and M3 and M4 muscarinic cholinergic receptors, which are both G protein-coupled receptors (GCPRs). 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.<ref>{{Cite web|url=https://www.meaction.net/2015/09/26/antibodies-found-in-subset-of-cfs-patients/|title=Autoantibodies found in subset of CFS patients {{!}} #MEAction|website=www.meaction.net|language=en-US|access-date=2018-08-12}}</ref><ref>{{Cite journal|last=Loebel|first=Madlen|author-link1=Madlen Löbel|last2=Grabowski|first2=Patricia|author-link2=Patricia Grabowski|last3=Heidecke|first3=Harald|last4=Bauer|first4=Sandra|author-link4=Sandra Bauer|last5=Hanitsch|first5=Leif G.|last6=Wittke|first6=Kirsten|last7=Meisel|first7=Christian|last8=Reinke|first8=Petra|last9=Volk|first9=Hans-Dieter|date=Feb 2016|title=Antibodies to β adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/26399744|journal=Brain, Behavior, and Immunity|volume=52|pages=32–39|doi=10.1016/j.bbi.2015.09.013|issn=1090-2139|pmid=26399744}}</ref>
Samples from a large cohort (n=268) in Berlin, Germany 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 receptor|adrenergic]] and M3 and M4 muscarinic cholinergic receptors, which are both G protein-coupled receptors (GCPRs). 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 [[biomarker]]s to those CFS patients most likely to respond to Rituximab treatment.<ref>{{Cite web|url=https://www.meaction.net/2015/09/26/antibodies-found-in-subset-of-cfs-patients/|title=Autoantibodies found in subset of CFS patients {{!}} #MEAction|website=www.meaction.net|language=en-US|access-date=2018-08-12}}</ref><ref>{{Cite journal|last=Loebel|first=Madlen|author-link1=Madlen Löbel|last2=Grabowski|first2=Patricia|author-link2=Patricia Grabowski|last3=Heidecke|first3=Harald|last4=Bauer|first4=Sandra|author-link4=Sandra Bauer|last5=Hanitsch|first5=Leif G.|last6=Wittke|first6=Kirsten|last7=Meisel|first7=Christian|last8=Reinke|first8=Petra|last9=Volk|first9=Hans-Dieter|date=Feb 2016|title=Antibodies to β adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/26399744|journal=Brain, Behavior, and Immunity|volume=52|pages=32–39|doi=10.1016/j.bbi.2015.09.013|issn=1090-2139|pmid=26399744}}</ref>


==Published Studies==
==Published Studies==

Revision as of 01:40, October 10, 2019

Theory[edit | edit source]

The Open Medicine Foundation, with immunologist Mark Davis, and geneticist Lars Steinmetz, is currently investigating the replication of T cells in ME, which may indicate an autoimmune disease is present in some ME/CFS patients.[1]

Evidence[edit | edit source]

Evidence for autoimmunity in ME and CFS[edit | edit source]

Shows fibromyalgia 30-77% overlap, Hashimoto's thyroiditis 17-20%, POTS 11-40% overlap and family history of autoimmune conditions 18-41% overlap.
Autoimmune conditions in people with ME/CFS. Source: Sotzny et al (2018), EUROMENE project.

Many people with ME/CFS also have autoimmune conditions such as Fibromyalgia or Hashimoto's thyroiditis, or have a family history of autoimmune diseases.[2] POTS, or postural orthostatic tachycardia syndrome, can be initiated or maintained by autoantibodies as well, and POTS is common in people with ME. A number of different immune system abnormalities have been found in some patients with ME/CFS.[2]

One study found elevated cellular antigens in 83% of CFS patients.[3]

Autoimmune disease is one of several illnesses or conditions experienced alongside of ME/CFS.[4]

Samples from a large cohort (n=268) in Berlin, Germany 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). 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.[5][6]

Published Studies[edit | edit source]

Talks & Interviews[edit | edit source]

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 Open Medicine Foundation (February 28, 2018). "OMF-funded research: T cells and molecular immunology". Open Medicine Foundation. Retrieved July 11, 2019. Cite has empty unknown parameter: |dead-url= (help)
  2. 2.0 2.1 2.2 Sotzny, Franziska; Blanco, Julià; Capelli, Enrica; Castro-Marrero, Jesús; Steiner, Sophie; Murovska, Modra; Scheibenbogen, Carmen (2018), "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome – Evidence for an autoimmune disease", Autoimmunity Reviews, 17 (6): 601-609, doi:10.1016/j.autrev.2018.01.009
  3. von Mikecz, A.; Konstantinov, K.; Buchwald, D. S.; Gerace, L.; Tan, E. M. (February 1997). "High frequency of autoantibodies to insoluble cellular antigens in patients with chronic fatigue syndrome". Arthritis and Rheumatism. 40 (2): 295–305. ISSN 0004-3591. PMID 9041942.
  4. "Overlapping Conditions – American ME and CFS Society". ammes.org. Retrieved August 12, 2018.
  5. "Autoantibodies found in subset of CFS patients | #MEAction". www.meaction.net. Retrieved August 12, 2018.
  6. Loebel, Madlen; Grabowski, Patricia; Heidecke, Harald; Bauer, Sandra; Hanitsch, Leif G.; Wittke, Kirsten; Meisel, Christian; Reinke, Petra; Volk, Hans-Dieter (February 2016). "Antibodies to β adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syndrome". Brain, Behavior, and Immunity. 52: 32–39. doi:10.1016/j.bbi.2015.09.013. ISSN 1090-2139. PMID 26399744.
  7. Morris, Gerwyn; Berk, Michael; Galecki, Piotr; Maes, Michael (April 1, 2014). "The Emerging Role of Autoimmunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/cfs)". Molecular Neurobiology. 49 (2): 741–756. doi:10.1007/s12035-013-8553-0. ISSN 1559-1182.
  8. Maes, Michael; Ringel, Karl; Kubera, Marta; Anderson, George; Morris, Gerwyn; Galecki, Piotr; Geffard, Michel (September 5, 2013). "In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation". Journal of Affective Disorders. 150 (2): 223–230. doi:10.1016/j.jad.2013.03.029. ISSN 0165-0327.
  9. Maes, Michael; Ringel, Karl; Kubera, Marta; Berk, Michael; Rybakowski, Janusz Rybakowski (February 1, 2012). "Increased autoimmune activity against 5-HT : a key component of depression that is associated with inflammation and activation of cell-mediated immunity, and with severity and staging of depression". Journal of affective disorders. 136 (3): 386–392. doi:10.1016/j.jad.2011.11.016. ISSN 0165-0327.
  10. Staines, Donald R (May 1, 2004). "Is chronic fatigue syndrome an autoimmune disorder of endogenous neuropeptides, exogenous infection and molecular mimicry?". Medical Hypotheses. 62 (5): 646–652. doi:10.1016/j.mehy.2004.01.012. ISSN 0306-9877.