Pathogenic T Cells in Guillain Barre Syndrome

Abstract

The human disease, Guillain Barre Syndrome (GBS), can be modeled in NOD.AireGW/+ mice that acquire an autoimmune peripheral neuropathy (APN). We have learned that APN in these mice requires UTX expression inCD4+ T cells. The goal of this project is to understand how UTX in T cells promotes APN, focusing on UTX's effects on gene expression in CD4+ T cells and the formation of pathogenic subsets of CD4+ T cells. In year 1, we worked toward understanding the role of UTX's demethylase domain in APN. In one series of experiments, NOD.AireGW/+ mice were treated with a compound that inhibits the UTX demethylase activity. We observed that this treatment failed to prevent APN, suggesting that UTX function is demethylase-independent. We also worked toward establishing a genetic model where APN-prone mice will express a mutant form of UTX that lacks demethylase activity.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2022
Accession Number
AD1193031

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  • Jason K Whitmire
  • Maureen A Su

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  • University of California, Los Angeles

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