Immunological mechanisms of the greatly increased risk of multiple sclerosis after Epstein-Barr virus infection / DMSG

The article from the Stanford University School of Medicine, California, by the working groups of Professor Lawrence Steinman and Dr. Bill Robinson, who studies the immune mechanisms. The basic finding of this research group is that a transcription factor EBNA1, which is essential for virus function and which expresses an EBV nuclear antigen-1 located in the cell nucleus, shows a very high molecular similarity (mimicry) of the protein structure with the cell adhesion protein GlialCAM found in the brain. This could be shown from structural mechanisms to the relevant function in living beings, supplemented by modern molecular techniques through to experimental transfer: A corresponding antibody from the cerebrospinal fluid was detected from B lymphocytes, both in the blood and in the cerebrospinal fluid of MS patients, and then verified accordingly on a protein expression library. Finally, the antibody could also be immunohistochemically bound to brain tissue sections, where it was shown that protein changes further increase binding to the GlialCAM protein. If you now go into the experimental model for multiple sclerosis, the experimental encephalomyelitis EAE, the course of the disease could be significantly worsened by immunization with EBNA1. This is a clear line of evidence that also mechanistically underpins the already published data from the Ascherio working group.



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