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ShRNA Knockdown of ILF3 in Monocyte-Derived Dendritic Cells (MDDCs)

ABSTRACT: Antigen presenting cells such as myeloid dendritic cells (DCs) are key sentinels of the innate immune system. In response to pathogen recognition and innate immune stimulation, DCs transition from an immature, inactive state to a mature, active state that is characterized by widespread changes in host gene expression. Several key transcription factors are known to drive these gene expression changes, but the mechanisms that negatively regulate DC maturation are less well understood. Here, we have identified that the transcription factor Interleukin Enhancer Binding Factor 3 (ILF3) is a negative regulator of innate immune responses and DC maturation. Depletion of ILF3 in primary human monocyte-derived DCs (MDDCs) using shRNA knockdown led to increased expression of maturation markers and potentiated innate responses at baseline.

ORGANISM(S): Homo sapiens

PROVIDER: GSE159458 | GEO | 2021/04/08

REPOSITORIES: GEO

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Project description:Human monocyte derived dendritic cells matured via galectin-1 or LPS. Experiment Overall Design: 4 conditions with 3 replicates of each include control or intreated immature MDDCS, galectin-1 treated MDDCs, LPS treated MDDCs, and vehicle control MDDCs. (each replicate is from a distinct DONOR). Dendritic cells (DCs) are potent mediators of the immune response, and can be activated by exogenous pathogen components. Galectin-1 is a member of the conserved beta-galactoside-binding lectin family that binds galactoside residues on cell surface glycoconjugates. Galectin-1 is known to play a role in immune regulation via action on multiple immune cells. However, its effects on human DCs are unknown. In this study, we show that galectin-1 induces a phenotypic and functional maturation in human monocyte-derived DCs (MDDCs) similar to but distinct from the activity of the exogenous pathogen stimuli, LPS. Immature human MDDCs exposed to galectin-1 up-regulated cell surface markers characteristic of DC maturation (CD40, CD83, CD86, and HLA-DR), secreted high levels of IL-6 and TNF-alpha, stimulated T cell proliferation, and showed reduced endocytic capacity, similar to LPS-matured MDDCs. However, unlike LPS-matured DCs, galectin-1-treated MDDCs did not produce the Th1-polarizing cytokine IL-12. Microarray analysis revealed that in addition to modulating many of the same DC maturation genes as LPS, galectin-1 also uniquely up-regulated a significant subset of genes related to cell migration through the extracellular matrix (ECM). Indeed, compared with LPS, galectin-1-treated human MDDCs exhibited significantly better chemotactic migration through Matrigel, an in vitro ECM model. Our findings show that galectin-1 is a novel endogenous activator of human MDDCs that up-regulates a significant subset of genes distinct from those regulated by a model exogenous stimulus (LPS). One unique effect of galectin-1 is to increase DC migration through the ECM, suggesting that galectin-1 may be an important component in initiating an immune response.

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ShRNA Knockdown of ILF3 in Monocyte-Derived Dendritic Cells (MDDCs)

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