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Fluorescence-activated Cell Sorting for Purification of Plasmacytoid Dendritic Cells from the Mouse Bone Marrow
Published on: November 4, 2016
Elevated expression of miR-142-3p is related to the pro-inflammatory function of monocyte-derived dendritic cells in
Yilun Wang1, Jun Liang2, Haihong Qin1
1Department of Dermatology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Road, Shanghai, 200040, People's Republic of China.
Background:
Recent studies have shown that alterations in the function of dendritic cells (DCs) are involved in the pathogenesis of systemic lupus erythematosus (SLE). However, the mechanism of the alteration remains unclear.
Methods:
We cultured monocyte-derived DCs (moDCs) in vitro and examined the cytokines and chemokines in the supernatants of moDCs in negative controls (NC) and SLE patients in active phase. We then profiled microRNAs (miRNAs) of LPS-stimulated moDCs in SLE patients and used real-time PCR to verify the differentially expressed miRNAs. A lentiviral construct was used to overexpress the level of miR-142-3p in moDCs of NC. We examined the cytokines and chemokines in the supernatants of moDCs overexpressing miR-142-3p and used Transwell test, flow cytometric analysis and cell proliferation to observe the impact on CD4+ T cells in moDC-CD4+T cell co-culture.
Results:
moDCs in patients with SLE secreted increased level of IL-6, CCL2 and CCL5, with attraction of more CD4+ T cells compared with NC. We found 18 differentially expressed microRNAs in moDCs of SLE patients by microarray, and target gene prediction showed some target genes of differentially expressed miRNAs were involved in cytokine regulation. miR-142-3p was verified among the highly expressed miRNAs in the SLE group and overexpressing miR-142-3p in moDCs of the NC group caused an increase of SLE-related cytokines, such as CCL2, CCL5, CXCL8, IL-6 and TNF-α. Moreover, moDCs overexpressed with miR-142-3p resulted in attraction of an increased number of CD4+ T cells and in suppression of the proportion of Tregs in DC-CD4+T cell co-culture whereas the proliferation of CD4+T cells was not altered.
Conclusions:
The results demonstrated a role for miR-142-3p in regulating the pro-inflammatory function of moDCs in the pathogenesis of SLE. These findings suggested that miR-142-3p could serve as a novel therapeutic target for the treatment of SLE.
Insights
MicroRNA-142-3p promotes inflammation in systemic lupus erythematosus (SLE) by altering dendritic cell (DC) function. This suggests miR-142-3p as a potential therapeutic target for SLE treatment.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Alterations in dendritic cell (DC) function are implicated in the pathogenesis of systemic lupus erythematosus (SLE).
- The precise mechanisms driving DC dysfunction in SLE remain incompletely understood.
Purpose of the Study:
- To investigate the role of microRNAs (miRNAs) in the altered function of monocyte-derived DCs (moDCs) in SLE.
- To elucidate the specific contribution of miR-142-3p to DC-mediated inflammation in SLE.
Main Methods:
- Cultured moDCs from SLE patients and healthy controls, analyzing cytokine and chemokine profiles.
- Performed miRNA profiling on LPS-stimulated moDCs to identify differentially expressed miRNAs.
- Overexpressed miR-142-3p in moDCs and assessed its impact on cytokine secretion and CD4+ T cell responses in co-culture systems.
Main Results:
- SLE moDCs exhibited elevated levels of IL-6, CCL2, and CCL5, attracting more CD4+ T cells.
- Microarray analysis revealed 18 differentially expressed miRNAs in SLE moDCs, with miR-142-3p being significantly upregulated.
- Overexpression of miR-142-3p in control moDCs increased pro-inflammatory cytokines (CCL2, CCL5, CXCL8, IL-6, TNF-α), enhanced CD4+ T cell attraction, and reduced Treg proportion without affecting T cell proliferation.
Conclusions:
- miR-142-3p plays a crucial role in regulating the pro-inflammatory functions of moDCs in SLE pathogenesis.
- These findings highlight miR-142-3p as a potential novel therapeutic target for managing SLE.
