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DC-specific lincRNA controls dendritic cell development and function through interacting with STAT3

ABSTRACT: To identify the functional non-coding RNAs in human DC development, we explored the gene expression profiles during DC development from peripheral monocytes. Using microarray technique, we identified many annotated lncRNAs with markedly altered expressions during human DC differentiation and maturation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE54143 | GEO | 2014/05/02

SECONDARY ACCESSION(S): PRJNA236563

REPOSITORIES: GEO

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DC-specific lincRNA controls dendritic cell development and function through interacting with STAT3

Project description:To identify the functional non-coding RNAs in human DC development, we explored the gene expression profiles during DC development from peripheral monocytes. Using microarray technique, we identified many annotated lncRNAs with markedly altered expressions during human DC differentiation and maturation. RNA samples from cells during the process of DC development from human peripheral blood monocytes were collected. Each time point sample was the pool of RNA from 3 donors.

2014-05-02 | E-GEOD-54143 | biostudies-arrayexpress

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Cdc42 controls DC-maturation - Cdc42-dependent actin dynamics controls maturation and secretory activity of dendritic cells

Project description:Cell division cycle 42 (Cdc42) is a member of the Rho GTPase family and has pivotal functions in actin organization, cell migration and proliferation. Cdc42 has been shown to regulate antigen (Ag)-uptake in immature dendritic cells (DC) and controls their migration from tissues to lymph nodes. Previous reports demonstrated that Cdc42 is inactivated upon DC-maturation to avoid continued Ag-acquisition. To further study the molecular mechanisms of DC-control by Cdc42, we used bone marrow-derived DCs from Cdc42-deficient mice. We show that Cdc42-deficient DCs are phenotypically mature without additional maturation stimuli, as they upregulate CD86 from intracellular storages to the cell surface. They also accumulate invariant chain (Ii)-MHC class II complexes at the cell surface, which cannot efficiently present peptide Ag for priming of Ag-specific CD4 T cells. Lack of Cdc42 in immature DCs does not allow MHC class II maturation, as lysosomal Cathepsins are lost into the supernatant and Ii-MHC class II complexes cannot mature. Therefore Cdc42-deficient DCs are "pseudomature" and lose most functional hallmarks of antigen-presenting cells. Our results propose that Cdc42 keeps DCs in an immature state, while downregulation of Cdc42-activity during maturation facilitates generation of CD86+MHCII+ mature DCs.

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