The Wistar Institute's Paul M. Lieberman, Ph.D., and lab team led by senior staff scientist and first author, Samantha Soldan, Ph.D.
May 28 2024The Wistar Institute The Wistar Institute's Paul M. Lieberman, Ph.D., and lab team led by senior staff scientist and first author, Samantha Soldan, Ph.D., have demonstrated how B cells infected with the Epstein-Barr virus can contribute to a pathogenic, inflammatory phenotype that contributes to multiple sclerosis ; the group has also shown how these problematic B cells can be selectively targeted in a way that reduces the damaging autoimmune response of multiple sclerosis .
Though researchers know that EBV can contribute to the development of MS, the exact mechanisms by which it does so aren't completely understood. The Lieberman lab, in seeking to understand how EBV contributes to the development of MS, collaborated with Steven Jacobson, Ph.D., of the Neuroimmunology Branch at the National Institute of Neurological Disorders and Stroke, who contributed cell line samples from patients.
Having obtained the matched samples, Dr. Lieberman and his team conducted genetic analyses of the SLCLs and confirmed that the MS-positive sample groups showed greater expression of genes associated with lytic EBV ; they also saw increased inflammatory signaling and expression of the FOXP1 protein, the latter of which was shown to promote lytic EBV gene expression. As a whole, the group's findings suggested a mechanism of lytic EBV in MS that promoted inflammation and disease.
Research Sclerosis Autoimmune Disease Brain Cell Cell Line Chronic Epstein-Barr Virus Gene Gene Expression Immune System Inflammation Microbiology Myelin Nervous System Neuroimmunology Neurons Ph Phenotype Stroke Virus
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