This study demonstrates that a large percentage of patients clinically diagnosed with CFS have elevated levels of the IgM isotype to CL (95%), suggesting that CFS may be an autoimmune condition. As a possible autoimmune disease, CFS patients may be treated by suppression of the ACA or by diminishing the antigen CL in serum. Previous studies have shown that treatment with monoclonal antibodies to B cells reduces ACA levels to normal in patients with autoimmune disease, leading to clinical improvements.
Specifically, Rituximab, a chimeric monoclonal CD20 antibody, has been shown to normalize high ACA serum titers of patients with autoimmune systemic lupus erythematosus, rheumatoid arthritis, autoimmune thrombocytopenia, and autoimmune hemolytic anemia. Rituximab may serve as an effective therapeutic agent for ameliorating the symptoms of CFS (11,13). Therefore, classification of CFS as an autoimmune disorder may serve to increase the availability of treatment options for patients suffering from the disease.
Experiments are underway to further elucidate why ACAs are produced in individuals afflicted with CFS.
Such studies include investigating the effects of specific chemical agents, marine toxins, and ACAs on mitochondrial metabolic pathways that are indicative of reduced or blocked energy production that may lead to the fatigued state in CFS. Such studies may lead to the development of potential therapeutic agents to block or reduce such interactions.
