

Publisher: John Wiley & Sons Inc
E-ISSN: 1098-1136|63|12|2231-2248
ISSN: 0894-1491
Source: GLIA, Vol.63, Iss.12, 2015-12, pp. : 2231-2248
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
The role and different origin of brain myeloid cells in the brain is central to understanding how the central nervous system (CNS) responds to injury. C‐type lectin receptor family 9, member A (DNGR‐1/CLEC9A) is a marker of specific DC subsets that share functional similarities, such as CD8α+DCs in lymphoid tissues and CD103+CD11blowDCs in peripheral tissues. Here, we analyzed the presence of DNGR‐1 in DCs present in the mouse brain (bDCs). Dngr‐1/Clec9a mRNA is expressed mainly in the meningeal membranes and choroid plexus (m/Ch), and its expression is enhanced by fms‐like tyrosine kinase 3 ligand (Flt3L), a cytokine involved in DC homeostasis. Using Clec9aegfp/egfp mice, we show that Flt3L induces accumulation of DNGR‐1‐EGFP+ cells in the brain m/Ch. Most of these cells also express major histocompatibility complex class II (MHCII) molecules. We also observed an increase in specific markers of cDC CD8α+ cells such as Batf‐3 and Irf‐8, but not of costimulatory molecules such as Cd80 and Cd86, indicating an immature phenotype for these bDCs in the noninjured brain. The presence of DNGR‐1 in the brain provides a potential marker for the study of this specific brain cell subset. Knowledge and targeting of brain antigen presenting cells (APCs) has implications for the fight against brain diseases such as neuroinflammation‐based neurodegenerative diseases, microbe‐induced encephalitis, and brain tumors such as gliomas. GLIA 2015;63:2231–2248
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