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Further research on EL-related antigens

 

 

Further research on possible EL-related antigens in the brain

 

The research on brain antigens that may be related to EL will continue in 2008 with a joint project at The Institute of Neurology, University College London, and The Institute of Cell and Molecular Science, Queen Mary University London, focusing on the  CNS distribution of a gamma/alpha-enolase, a putative auto-antigen recognised by anti-basal ganglia antibodies in subjects with encephalitis lethargica. This research aims to examine whether gamma/alpha-enolase dimers are enriched in the basal ganglia, and eventually to determine whether autoantibodies to these dimers are associated with encephalitis. Professor Giovannoni writes:

We and others have identified an emerging group of autoimmune diseases of the CNS characterised by the presence of anti-basal ganglia antibodies (ABGAs) that are associated with recent streptococcal infection. The spectrum of neuropsychiatric disorders associated with ABGA and streptococcal infection includes encephalitis lethargica, Sydenham’s chorea, PANDAS, Tourette’s syndrome, adult-onset tics, dystonia and obsessive-compulsive disorder. In the human basal ganglia ABGA recognise four main bands of 40, 45, 60 and 98 kDa. We have purified and identified all these antigens. The 45 and 98 kDa antigens are the monomeric and dimeric forms of gamma-enolase and alpha-enolase, the 40 kDa antigen is aldolase C (neurone specific) and the 60 kDa antigen is pyruvate kinase M1. All the antigens are glycolytic enzymes and are involved in energy homeostasis and, as expected, are found in the cytosol. These proteins are also located on the neuronal surface, where they appear to have alternative functions. For example, enolase located on the surface of neurones acts as a receptor for plasmin/plasminogen and has been shown to be a trophic factor for dopaminergic neurones. All these enzymes are found in lipid rafts and may interact with other membrane proteins, e.g. ion channels. These autoantigens are therefore good candidates to be involved in the pathogenesis of ABGA-associated disorders. All these putative autoantigens have homologous proteins in streptococci. We now have preliminary evidence that ABGAs are induced by molecular mimicry. The 98 kDa antigen or gamma/alpha-enolase dimer is particularly interesting in that it is also expressed in the heart and appears to be purely a membrane protein.

 

 
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