Hamster Anti-Mouse Itgax Heterohybridoma [O529]

Dendritic cells (DC) are specialized antigen-presenting cells, responsible for peripheral immune responses. Recently, resident brain dendritic cells (bDC) were identified and functionally characterized in the young adult Itgax (CD11c) EYFP+ transgenic mouse brain. In the present study, we describe changes in number, phenotype, and source of bDC in the aging mouse brain. Immunohistochemistry and fluorescent activated cell sorting (FACS) analysis revealed an age-related increase in bDC with a concomitant rise in the expression of immune activation markers MHCII, CD80, and CD86. Quantification of immunolabeled bDC in the cortex, corpus callosum, and cerebellum of the aged brain revealed a 2- to 5-fold increase. In contrast, either no change or a decrease in bDC was noted in regions of adult neurogenesis. Chimeras (wild type host/EYFP+ bone marrow) suggest that the increase of EYFP+ cells in the aging brain is in part due to an accumulation of peripherally derived cells. Collectively, the numerical and phenotypic changes in bDC indicate these cells may serve as an important immune component in the functional and anatomic alterations associated with aging. (C) 2012 Elsevier Inc. All rights reserved.

Adipose tissue derived chronic inflammation is a critical component of obesity induced type II diabetes. Major histocompatibility complex II (MHCII) mediated T cell activation within adipose tissue is one mechanism that contributes to this phenotype. However, the contribution of dendritic cells as professional antigen presenting cells in adipose issue has not previously been explored. Using Itgax(Cre) x MHCIIfl/fl (M11cKO) mice we observed adipose tissue specific changes in adipose tissue leukocytes. While there was a complete knockout of MHCII in dendritic cells, MHCII was also absent on the majority of macrophages. This resulted in reduction of TCR expression in CD4(+) T cells in obese adipose tissue, and an increase in CD8(+) and CD4(+) CD8(+) double positive T cells with decreased CD4(+) T cells independent of diet type. Increased CD8(+) cells were not observed in the spleen, suggesting adipose tissue T cell regulation is tissue specific. In vitro studies demonstrated more potent antigen presentation function in adipose tissue dendritic cells compared to macrophages. Obese M11cKO mice had decreased CD11c(+) adipose tissue macrophages. Despite the changes of immune cellularity in adipose tissue, M11cKO largely did not change inflammatory gene expression in adipose tissue and did not demonstrate differences in glucose and insulin intolerance. Overall MHCII expression on CD11c(+) cells is important for maintaining CD4(+) and CD8(+) adipose tissue T cells, but these cellular changes fail to alter inflammatory output and systemic metabolism.