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- W1551004966 abstract "Abstract Bcl-3 is a nuclear member of the family of IκB inhibitors; it can act as an activator or inhibitor of NF-κB activity, depending on the context, and it functions via association with homodimers of the p50 or p52 subunits of NF-κB. In recent years various NF-κB subunits have been implicated in the development and activation of dendritic cells (DCs), which are important effectors in the activation of the innate and adaptive immune system. Here we have explored, for the first time, the role of Bcl-3 in DC-mediated functions. We report that Bcl-3 is required to prime CD4 T cells in vitro. By using an OT-II adoptive transfer model, we were able to demonstrate that Bcl-3 deficient DCs lacked the capacity to prime T cells in vivo. Furthermore, specific ablation of Bcl-3 in DCs in vivo, revealed that Bcl-3 is required for the development of contact hypersensitivity reactions. Mechanistically, Bcl-3 is dispensable for DC maturation and inflammatory cytokine production. In conclusion, we demonstrated for the first time that Bcl-3 expression in DCs is required for the initiation of the adaptive immune response in vitro and in vivo." @default.
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- W1551004966 date "2012-05-01" @default.
- W1551004966 modified "2023-09-27" @default.
- W1551004966 title "Bcl-3 is a regulator of dendritic cell functions (172.30)" @default.
- W1551004966 doi "https://doi.org/10.4049/jimmunol.188.supp.172.30" @default.
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