During the postdoctoral appointment at the National Institutes for Health, we extensively characterized the gene profile of TLR agonist-stimulated immune cells from patients suffering from ectodermal dysplasia with immune deficiency. We identified several NF-κB responsive elements, which supposedly participates to intracellular organization and activation of antigen-presenting cells. Recent progresses made in the comprehension of the mechanisms responsible for eliciting innate responses, point out the key role of a multi-molecular platform, called inflammasome. In response to several danger signals, the inflammasome promotes the release of pro-inflammatory cytokines, such as IL-1β. A few hints suggest that one of our NF-κB regulated proteins might participate to the inflammasome activation. Using the Cre-lox technology, we will generate a conditional deficient mouse for the gene candidate in CD11c expressing cells. With this animal model, we expect to define the precise role played by NF-κB target genes in antigen-presenting cell biology and discover new mechanisms that shape immune responses following antigen detection.