title: Comment on "Activation of β-catenin in dendritic cells regulates immunity versus tolerance in the intestine".
abstract: Manicassamy et al. (Reports, 13 August 2010, p. 849) deleted β-catenin in intestinal immune cells using a CD11c-driven Cre recombinase, which decreased anti-inflammatory mediators and increased inflammatory bowel disease. However, the deletion of β-catenin in macrophages remains a caveat to their interpretation that Wnt signaling programs dendritic cells into a tolerogenic state. Development of strains expressing Cre in a more finely lineage-restricted pattern may help resolve this issue.
authors.affiliation: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. kmurphy@wustl.edu
authors.forename: Kenneth M
authors.initials: KM
authors.lastname: Murphy
mesh_terms: D000818:Animals; D039521:CD11c Antigen / Q000032:analysis / Q000235:genetics; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D017353:Gene Deletion; D007108:Immune Tolerance; D019426:Integrases / Q000378:metabolism; D007422:Intestines / Q000276:immunology*; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D011995:Recombination, Genetic; D015398:Signal Transduction; D051176:beta Catenin / Q000235:genetics* / Q000378:metabolism*
chemical_list: D039521:CD11c Antigen; C495267:CTNNB1 protein, mouse; D051176:beta Catenin; C045073:Cre recombinase; D019426:Integrases