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- W2096531164 abstract "RATIONALE: The ability of CD40 signaling to regulate B cell growth, survival, differentiation, and Ig class switching involves changes in gene expression. CD40 ligation activates the Rel/NF-κB transcription factors, which are major regulators of immune and inflammatory responses and potentially activates both type 1 (p105/p50) and type 2 (p100/p52) NF-κB activation pathways. Using primary B cells, we investigated the contribution of NFκb activation on CD40 mediated IL-13 receptor expression, using BAY11, an IkappaB-alpha phosphorylation inhibitor. METHODS: Human B lymphocytes were isolated from tonsils and purified by sheep red blood cell rosetting. B cells were stimulated with anti-CD40 antibodies and nuclear extracts prepared from B cells were assayed for p50 and p52 activity using the TransAM NFκB Family Kit, or Western blotting. We observed the effects of BAY11 on NF-κB activation, phosphorylation of IkappaB-alpha, and nuclear translocation of NF-κB subunits. IL-13R expression and IL-13 mediated STAT6 signalling were monitored by flow cytometry. RESULTS: BAY11 significantly decreased both anti-CD40 induced IL-13 receptor mRNA and IL-13 receptor surface expression. It also inhibited the ability of IL-13 to induce STAT6 following CD40 ligation. This was associated with Bay 11 inhibiting CD40-mediated phosphorylation of IkappaB-alpha, an upstream effector of p50. CD40 rapidly induces p50 processing within 5 min; pretreatment of B cells with Bay11 inhibited the activation of p50 induced by CD40L. CONCLUSIONS: This data show that CD40L-induced IL-13 receptor expression is NFκB dependent, involving preferentially the (p105/p50) NF- B1pathway. Inhibition of IL-13R expression and its ability to signal can be effected by blocking CD40 signal transduction via NFκb." @default.
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- W2096531164 date "2006-02-01" @default.
- W2096531164 modified "2023-09-27" @default.
- W2096531164 title "Induction of Interleukin-13 Receptor Expression Via Nuclear Factor-Kappab Activation in Human Tonsillar B Cells" @default.
- W2096531164 doi "https://doi.org/10.1016/j.jaci.2005.12.584" @default.
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