Autoantibodies and pain

Over the last 20 years, several neurological conditions have been identified which appear to be caused directly by autoantibodies targeting receptors, ion channels and related proteins on neuronal or glial cells. Neuroimmune interactions are now accepted contributors to chronic pain conditions. Autoantibodies might be one such cause and here we highlight their potential role in pathological pain.

Recent studies have given more weight to the idea that autoantibodies can be directly related to pain; this is suggested by the success of immunotherapy in patients and preclinical studies in animal models. For example, in complex regional pain syndrome, plasma exchange or intravenous immunoglobulins have been successful in reducing pain scores. Similarly, immunotherapies reduce autoantibody levels and pain in neuromyelitis optica and voltage-gated potassium channel complex antibody positive patients. Furthermore, animal studies show that IgG autoantibodies from patients with rheumatoid arthritis or complex regional pain syndrome can recapitulate pain phenotypes in mice.

There is growing evidence that some pain syndromes may be caused by autoantibodies to proteins that modify or exacerbate pain sensation. This has potentially direct therapeutic advantages for these patients and possible wider implications for sufferers of chronic pain more generally.