Essential Roles of c-Rel in TLR-Induced IL-23 p19 Gene Expression in Dendritic Cells

摘要: IL-23 plays crucial roles in both immunity against pathogens and autoimmunity self. Although it is well recognized that expression restricted to the myeloid lineage tightly regulated at transcriptional level, nature of transcription factors required for poorly understood. We report, this study, murine dendritic cells deficient c-Rel, a member NF-kappaB family, are severely compromised their ability transcribe p19 gene, one two genes encode protein. The gene promoter contains three putative binding sites, which can effectively bind c-Rel as determined by chromatin immunoprecipitation EMSA. Unexpectedly, mutation either these sites completely abolished activity induced five TLRs (2, 3, 4, 6, 9) four members family (c-Rel, p65, p100, p105). Based on observations, we conclude controls through kappaB promoter, propose c-Rel-dependent enhanceosome model activation.