Impaired Bcl3 Up-regulation Leads to Enhanced Lipopolysaccharide-induced Interleukin (IL)-23P19 Gene Expression in IL-10–/– Mice

摘要: Genetic and biochemical analyses show that IL-23p19 plays a central role in mediating bacteria-induced colitis interleukin-10-deficient (IL-10–/–) mice. The molecular mechanisms responsible for the dysregulated innate host response leading to enhanced IL-23 gene expression IL-10–/– mice are poorly understood. In this study, we investigated of Bcl3 controlling LPS-induced bone marrow-derived dendritic cells (BMDC) isolated from We report higher mRNA accumulation protein secretion LPS-stimulated BMDC compared with WT Lipopolysaccharide (LPS)-induced B cell leukemia 3 (Bcl3) was strongly impaired (90% decrease) BMDC. Chromatin immunoprecipitation demonstrated RelA binding promoter overexpression decreased BMDC, which correlated NF-κB p50 promoter. Conversely, knockdown Moreover, significantly Bcl3–/– conclusion, is due diminished recruitment