{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cohen SB"],"funding":["NIAID NIH HHS"],"pagination":["210-22"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4333072"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["194(1)"],"pubmed_abstract":["Beta-catenin signaling has recently been tied to the emergence of tolerogenic dendritic cells (DCs). In this article, we demonstrate a novel role for beta-catenin in directing DC subset development through IFN regulatory factor 8 (IRF8) activation. We found that splenic DC precursors express beta-catenin, and DCs from mice with CD11c-specific constitutive beta-catenin activation upregulated IRF8 through targeting of the Irf8 promoter, leading to in vivo expansion of IRF8-dependent CD8a+, plasmacytoid, and CD103+ CD11b2 DCs. beta-catenin–stabilized CD8a+ DCs secreted elevated IL-12 upon in vitro microbial stimulation, and pharmacological beta-catenin inhibition blocked this response in wild-type cells. Upon infections with Toxoplasma gondii and vaccinia virus, mice with stabilized DC beta-catenin displayed abnormally high Th1 and CD8+ T lymphocyte responses, respectively. Collectively, these results reveal a novel and unexpected function for beta-catenin in programming DC differentiation toward subsets that orchestrate proinflammatory immunity to infection."],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Beta-catenin signaling drives differentiation and proinflammatory function of IRF8-dependent dendritic cells."],"pmcid":["PMC4333072"],"funding_grant_id":["R01 AI110613","R21 AI109061","R56 AI083405","R01 AI083405"],"pubmed_authors":["McDougal C","Smith NL","Pepper M","Clausen BE","Cohen SB","Shah S","Jiang A","Rudd BD","Yap GS","Denkers EY","Acha-Orbea H"],"additional_accession":[]},"is_claimable":false,"name":"Beta-catenin signaling drives differentiation and proinflammatory function of IRF8-dependent dendritic cells.","description":"Beta-catenin signaling has recently been tied to the emergence of tolerogenic dendritic cells (DCs). In this article, we demonstrate a novel role for beta-catenin in directing DC subset development through IFN regulatory factor 8 (IRF8) activation. We found that splenic DC precursors express beta-catenin, and DCs from mice with CD11c-specific constitutive beta-catenin activation upregulated IRF8 through targeting of the Irf8 promoter, leading to in vivo expansion of IRF8-dependent CD8a+, plasmacytoid, and CD103+ CD11b2 DCs. beta-catenin–stabilized CD8a+ DCs secreted elevated IL-12 upon in vitro microbial stimulation, and pharmacological beta-catenin inhibition blocked this response in wild-type cells. Upon infections with Toxoplasma gondii and vaccinia virus, mice with stabilized DC beta-catenin displayed abnormally high Th1 and CD8+ T lymphocyte responses, respectively. Collectively, these results reveal a novel and unexpected function for beta-catenin in programming DC differentiation toward subsets that orchestrate proinflammatory immunity to infection.","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Jan","modification":"2025-04-21T21:18:35.441Z","creation":"2019-03-27T01:46:41Z"},"accession":"S-EPMC4333072","cross_references":{"pubmed":["25416805"],"doi":["10.4049/jimmunol.1402453"]}}