Myalgic Encephalomyelitis/Chronic Fatigue Syndrome – Evidence for an autoimmune disease by Franziska Sotznya, Julià Blancob, Enrica Capellid, Jesús Castro-Marrerof, Sophie Steinera, Modra Murovskag, Carmen Scheibenbogen in Autoimmun Rev. 2018 Apr 7. pii: S1568-9972(18)30088-0. [Epub ahead of print]
- The pathogenesis of ME/CFS is multifactorial, and immunological and environmental factors play a role.
- Autoimmune mechanisms can be linked with ME/CFS at least in a subset of patients.
- Autoantibodies mostly against nuclear and neurotransmitter receptors are found in a subset of ME/CFS patients.
- Immunomodulatory therapeutic strategies targeting autoantibodies may be beneficial and should be pursued.
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a frequent and severe chronic disease drastically impairing life quality. The underlying pathomechanism is incompletely understood yet but there is convincing evidence that in at least a subset of patients ME/CFS has an autoimmune etiology.
In this review, we will discuss current autoimmune aspects for ME/CFS. Immune dysregulation in ME/CFS has been frequently described including changes in cytokine profiles and immunoglobulin levels, T- and B-cell phenotype and a decrease of natural killer cell cytotoxicity. Moreover, autoantibodies against various antigens including neurotransmitter receptors have been recently identified in ME/CFS individuals by several groups.
Consistently, clinical trials from Norway have shown that B-cell depletion with rituximab results in clinical benefits in about half of ME/CFS patients. Furthermore, recent studies have provided evidence for severe metabolic disturbances presumably mediated by serum autoantibodies in ME/CFS. Therefore, further efforts are required to delineate the role of autoantibodies in the onset and pathomechanisms of ME/CFS in order to better understand and properly treat this disease.