Dr Madlen Löbel & Prof. Carmen Scheibenbogen
Institute of Medical Immunology, Charité University Medicine Berlin, Berlin, Germany
Antibodies are proteins produced by our immune system which can recognise and attack harmful invaders such as bacteria and viruses. Autoantibodies, on the other hand, occur when the immune system wrongly identifies the body’s own healthy cells as harmful and produces antibodies against them. This can lead to the development of a so-called autoimmune disease such as multiple sclerosis or lupus.
A couple of recent findings suggest that autoantibodies may also have a role in ME/CFS, at least in some patients.
Firstly, autoantibodies against adrenergic receptors (which are involved in the sympathetic nervous system) have been found in people with postural orthostatic tachycardia syndrome or orthostatic hypotension, disorders also seen in ME/CFS patients.
And secondly, two clinical trials of the antibody rituximab (which attacks B cells and is often used to treat autoimmune conditions) in ME/CFS patients reported significant benefits to around 60% of participants. Their responses were delayed by five months, suggesting that the clinical effects of rituximab only occurred when the autoantibodies produced by the B cells had been washed out.
In 2016, Dr Madlen Löbel and Prof. Carmen Scheibenbogen at the Institute of Medical Immunology in Berlin found that nearly a third of ME/CFS patients they studied had increased levels of autoantibodies against adrenergic receptors. Furthermore, these levels decreased in individuals who responded to treatment with rituximab.
This unexpected finding suggests that, in a subgroup of patients, some of the symptoms of ME/CFS may be caused by these autoantibodies, although their exact role in the illness is not yet clear.
ME Research UK has therefore awarded funding to Dr Löbel and Prof. Scheibenbogen to continue their investigations by looking at the function of β2 adrenergic receptor autoantibodies in ME/CFS.
They will identify patients with these autoantibodies and those without, and compare a wide range of clinical and immunological measures between the two groups. These measures will include clinical symptoms such as fatigue, physical function and signs of autonomic dysfunction, as well as blood vessel function, immune marker expression, and the proliferation of T and B cells.
In this way, the researchers hope to discover which of these symptoms and immune abnormalities might be affected by the presence of these potentially harmful autoantibodies.