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- W41609908 abstract "Abstract Our previous studies have demonstrated a CD40 signaling defect in B cells from a patient with non-X-linked HIGM (pt1). To elucidate the cause for impaired CD40 signals, we utilized a mini-EBV transformed cell line with inducible latent membrane protein 1 (LMP1) expression (LCLtet). The LMP1 signaling pathway appears to be intact, however CD40 activation was unable to promote cell division and transcriptional synthesis of cMyc in pt1-LCLtet cells. We examined mediators of the CD40 signaling pathway and found impaired localization of CD40 to microdomains, thereby impeding TNF receptor-associated factor recruitment and degradation after 2h of CD40 activation. However, prolonged CD40 ligation was sufficient to induce proper CD40 distribution, suggesting that the pt1 B cells possess a higher CD40 activation threshold that requires a greater magnitude of extensive and sustained CD40 signals to achieve signal transmission. Furthermore, pt1 B cells have a unique CD40 expression profile, indicative of an isoform with post-translational modifications. Specifically, CD40 on pt1 B cells is constitutively hyperphosphorylated and not differentially regulated by LMP1 or CD40 signals. These data collectively suggest that modulation of post-translational modifications, which mediate CD40 function and activity, may provide further insight into the cause of defective CD40 signals in this unique form of HIGM. (AI37081)" @default.
- W41609908 created "2016-06-24" @default.
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- W41609908 date "2007-04-01" @default.
- W41609908 modified "2023-09-25" @default.
- W41609908 title "Modifications of CD40 regulate defective CD40 signals in B cells from a patient with non-X-linked hyper IgM syndrome (HIGM) (35.13)" @default.
- W41609908 doi "https://doi.org/10.4049/jimmunol.178.supp.35.13" @default.
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