Anti-neuronal autoimmunity in Lyme disease

Neurological sequelae of chronic Lyme disease include encephalopathy, myelopathy and peripheral neuropathy. These have generally been attributed to either persistent infection or pathogen-induced autoimmunity (IOM, Institute of Medicine, 2011)↑. […]

paolo maccallini

Introduction

Neurological sequelae of chronic Lyme disease include encephalopathy, myelopathy and peripheral neuropathy. These have generally been attributed to either persistent infection or pathogen-induced autoimmunity (IOM, Institute of Medicine, 2011).

Anti-HSP60 antibodies

In 1988, Sigal et al. found that sera from patients with neurological manifestations of Lyme disease had IgM antibodies that bound to normal human axons, whereas binding was absent or weak in patients without neurologic findings (Sigal, et al., 1988). In 1993, Dai et al. proved that a monoclonal antibody (H9724) specific for the 41-kDa flagellar protein of Borrelia burgdorferi, cross-reacted with human axons. The cross-reacting protein was identified as chaperonin-HSP60 (Dai, et al., 1993). It was also proven in the same year, that human sera from Lyme patients which bound to human axons, also bound to HSP60 (Sigal, 1993). In 2001, evidence was provided that addition of H9724 to…

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