Differentially expressed microRNAs regulate plasmacytoid vs. conventional dendritic cell development

Mononuclear phagocyte miRNome analysis identifies miR-142 as critical regulator of murine dendritic cell homeostasis

“…24 Similarly, miR-196b and miR-221/ 222 were highly expressed in replicating progenitors, which may be linked to their reported function in leukemia pathogenesis. 44,45 However, in contrast to a previous study, we could not detect higher levels of these miRNAs in the cDC compartment compared with pDCs, 43 highlighting differences between ex vivo isolates and in vitro-cultured cells. BM Ly6C ϩ monocytes showed a less specific miRNA expression pattern compared with MPs and DCs, but interestingly characterized by a complete absence of miR-155 expression and prominent expression of the miR-23aϳmiR-24 cluster.…”

“…Therefore, although miR-146a and miR-223 were shown to have a functional impact on DCs and neutrophils, respectively, 21,22 their absence does not seem to affect the development of these cells. In addition, the analysis of CD11c-Cre:Dicer fl/fl mice generated to address the general role of miRNAs in cDCs yielded limited insights, 43 most likely because of a complicated interplay among the unknown average miRNA half-life, the time needed for the CD11c-promotercontrolled Cre recombinase-mediated loss of Dicer, and the limited cDC lifespan.…”

The equivalents of human blood and spleen dendritic cell subtypes can be generated in vitro from human CD34+ stem cells in the presence of fms-like tyrosine kinase 3 ligand and thrombopoietin

“…This established culture system has enabled detailed studies of the specialized function and development of murine DC subsets. [8][9][10][11] The study of human DC has lagged behind. Initial studies on human DC have focused on DC found in blood.…”

Functional regulation of monocyte-derived dendritic cells by microRNAs

“…Lack of DC phenotypes is proposed to be due to the short life span of resident DCs and long half-life of miRNAs (Kuipers et al, 2010b), it could also be that deletion of Dicer in CD11c + cells is too late to affect DC differentiation from CD11c -precursors. Nevertheless, in vitro manipulation of miRNA expression in DC precursors can change development fate of normal DCs (Kuipers et al, 2010a). We also found that blocking biosynthesis of miRNAs in DC precursors with inducible deletion of Drosha perturbed DC differentiation in vitro and in vivo (YZ, unpublished data).…”

“…Within hematopoietic cells, miRNAs are differentially expressed by different lineages of hematopoietic cells (Chen et al, 2004). Within DC lineages, the miRNA expression pattern is also unique between DC subsets (Kuipers et al, 2010a). For the same type of DCs, expression of miRNAs can also change during activation (Ceppi et al, 2009;Sun et al, 2011).…”