17β-Estradiol Alters the Activity of Conventional and IFN-Producing Killer Dendritic Cells

• DOI: 10.4049/jimmunol.180.3.1423
• Publication Date: 2014-04-18T22:54:53Z
• Authors: Mark C Siracusa; Michael G Overstreet; Franck Housseau; Alan L Scott; Sabra L Klein
• Keywords: CD11c; Follicular dendritic cells; CD86; CD49b

Abstract Estrogens increase aspects of innate immunity and contribute to sex differences in the prevalence autoimmune diseases response infection. The goal present study was assess whether exposure 17β-estradiol (E2) affects development function bone marrow-derived dendritic cells determine similar changes are observed CD11c+ splenocytes exposed E2 vivo. facilitated differentiation BM precursor into functional CD11c+CD11b+MHC class II+ (DCs) with increased expression costimulatory molecules CD40 CD86. Exposure also enhanced production IL-12 TLR ligands, CpG LPS. In contrast, isolated from spleens female C57BL/6 mice that were intact, ovariectomized, or ovariectomized replacement exhibited no number activity DCs. presence vivo, however, CD11c+CD49b+NK1.1low reduced numbers CD11c+CD49b+NK1.1high cells, a surface phenotype for IFN-producing killer DCs (IKDCs). Ultrastructural analysis demonstrated CD11c+NK1.1+ populations comprised had appearance both IKDCs. animals supplemental produced more IFN-γ IL-18. These data illustrate has differential effects on IKDCs provide evidence may strengthen by enhancing cells.