To address the role of cDCs in the progression of AD-like inflammation, we generated a mouse model that constitutively lacks CD11chi cDCs (30) by crossing CD11c-Cre bacterial artificial chromosome (BAC) Tg mice (CD11c-Cre mice) (31) to mice that harbor the diphtheria toxin (DT) α chain (DTA) under control of a loxP-flanked stop cassette in the ubiquitously expressed ROSA26 locus (R-DTA mice) (32) to produce CD11c-Cre:R-DTA double-Tg mice, referred to as CD11c-Cre:R-DTA mice. This evidence concerns the gene ITGAX and Alzheimer disease.