novel b cell-dependent multiple sclerosis model using extracellular domains of myelin proteolipid protein

Clicks: 149
ID: 140469
2020
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Ranked #92 of 107 articles by views in historia de la educación

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Abstract
Abstract Therapeutic success of B cell-targeting approaches in multiple sclerosis (MS) has intensified research into the pathogenic and regulatory roles these cells play in demyelinating disease. Dissecting the function of B cells in the MS mouse model experimental autoimmune encephalomyelitis (EAE) is largely confined to induction with either the myelin oligodendrocyte glycoprotein epitope MOG35–55 or the full-length recombinant human MOG protein, the latter representing the most-used B cell-dependent EAE model. There is a clear need to investigate B cell function in additional myelin antigen contexts. Unlike MOG35–55, where lack of B cells yields more severe disease, we show here that the immunodominant myelin proteolipid protein epitope (PLP178–191) elicited identical EAE in WT and μMT mice, suggesting an absence of B cell engagement by this peptide. We hypothesized that a longer PLP antigen may better engage B cells and designed a peptide encompassing the extracellular domains (ECD) of PLP. We demonstrate here that PLPECD-immunized B cell-deficient mice failed to exhibit EAE. In contrast, PLPECD induced EAE not only in WT mice, but in B cell-sufficient mice incapable of secreting antibodies, suggesting a predominant antigen presentation role. These results establish a novel, efficient B cell-dependent EAE model.
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boyden2020scientificnovel Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Alexander W. Boyden;Ashley A. Brate;Nitin J. Karandikar
Journal historia de la educación
Year 2020
DOI
10.1038/s41598-020-61928-w
URL
http://link.springer.com/article/10.1038/s41598-020-61928-w
Keywords
medicinescience

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