Volume 17, Issue 6, June 2018, Pages 601-609
Review: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome – Evidence for an autoimmune disease
Under a Creative Commons license open access
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 (MECFS) 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 MECFS has an autoimmune etiology. In this review, we will discuss current autoimmune aspects for MECFS. Immune dysregulation in MECFS 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 MECFS 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 MECFS patients. Furthermore, recent studies have provided evidence for severe metabolic disturbances presumably mediated by serum autoantibodies in MECFS. Therefore, further efforts are required to delineate the role of autoantibodies in the onset and pathomechanisms of MECFS in order to better understand and properly treat this disease.