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- W4313383018 abstract "Abstract The gene encoding the co-stimulatory molecule CD137 is located within the Idd9.3 T1D susceptibility locus and contributes to diabetes progression in NOD mice. We have previously shown that CD137 expression in T cells has dual functions: CD4+CD137+ T cells inhibited T1D development while CD8+CD137+ T cells showed potent diabetogenecity. The protective function of CD137 in CD4+T cells is likely due to the significant amounts of soluble CD137 (sCD137) produced by Foxp3+ Tregs. sCD137 is an alternatively spliced form of CD137 lacking the transmembrane encoding exon. Treating NOD mice with recombinant sCD137 prevents T1D development. We aim to study the impact of CD137 ligand on the expression of sCD137. We used CRISPR/Cas9 to generate a strain of NOD depleted of CD137L (NOD.Tnfsf9−/−). Development of T1D was repressed in the newly generated strain. Deficiency of CD137L was associated with increased levels of serum sCD137. CD137-deficient-T cells contributed significantly to the elevated serum levels of sCD137. Ligand-deficient-Treg cells produced higher levels of sCD137 proteins compared to wild-type Tregs. Moreover, we detected increased levels of sCD137 transcripts in Tregs lacking the expression of CD137L. We direct our efforts to uncover the molecular mechanisms involved in the regulatory role of CD137L influencing the expression of sCD137." @default.
- W4313383018 created "2023-01-06" @default.
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- W4313383018 date "2019-05-01" @default.
- W4313383018 modified "2023-09-28" @default.
- W4313383018 title "The absence of CD137 ligand upregulates the expression of the immunosuppressive molecule soluble CD137" @default.
- W4313383018 doi "https://doi.org/10.4049/jimmunol.202.supp.116.9" @default.
- W4313383018 hasPublicationYear "2019" @default.
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