title: Autoantibody pain.
abstract: As autoantibodies bind to target tissues, Fc-region dependent inflammation can induce pain via mediators exciting nociceptors. But recently another possibility has emerged, where autoantibody binding to nociceptors can directly cause pain, without inflammation. This is thought to occur as a result of Fab-region mediated modification of nerve transduction, transmission, or neuropeptide release. In three conditions, complex regional pain syndrome, anti-voltage gated potassium channel complex autoimmunity, and chronic fatigue syndrome, all associated with no or only little inflammation, initial laboratory-, and clinical trial-results have suggested a potential role for autoantibody-mediated mechanisms. More research assessing the pathogenic roles of autoantibodies in these and other chronic pain conditions is required. The concept of autoantibody-mediated pain offers hope for the development of novel therapies for currently intractable pains.
authors.affiliation: Pain Research Institute, Department of Translational Medicine, University of Liverpool, and The Walton Centre NHS Foundation Trust, Liverpool, L9 7AL, UK. Electronic address: andreasgoebel@rocketmail.com.
authors.forename: Andreas
authors.initials: A
authors.lastname: Goebel
mesh_terms: D001323:Autoantibodies / Q000276:immunology*; D002908:Chronic Disease; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D009437:Neuralgia / Q000209:etiology*
chemical_list: D001323:Autoantibodies
keywords: Autoantibody; CRPS; Chronic fatigue syndrome; Complex regional pain syndrome; Neuropathic pain; Pain; Voltage gated potassium channels