{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tang HC"],"funding":["National Natural Science Foundation of China"],"pagination":["1379458"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7320286"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["2020"],"pubmed_abstract":["<h4>Background</h4>The role of miR-223-3p in dendritic cells (DCs) is unknown. This study is aimed at investigating the effect of miR-223-3p on the antigen uptake and presentation capacities of DCs and the underlying molecular mechanism.<h4>Methods</h4>FITC-OVA antigen uptake and cell surface markers in bone marrow-derived DCs (BMDCs) were analyzed by flow cytometry. BMDCs were transfected with the miR-223-3p mimic or inhibitor. Cytokine levels were determined by ELISA. CD4+ T cell differentiation was determined by mixed lymphocyte culture assay.<h4>Results</h4>OVA treatment significantly downregulated miR-223-3p in BMDCs. The miR-223-3p mimic significantly inhibited OVA-induced antigen uptake and surface expression of MHC-II on BMDCs (<i>P</i> < 0.01). The miR-223-3p mimic increased TGF-<i>β</i>1 production in OVA-treated DCs (<i>P</i> < 0.01). Mixed lymphocyte reaction showed that the miR-223-3p mimic significantly promoted Treg cell differentiation. In addition, the miR-223-3p mimic significantly upregulated CD103 in DCs, indicating the promotion of tolerogenic DCs. The miR-223-3p mimic downregulated Rhob protein in OVA-induced DCs. Rhob knockdown significantly suppressed the ability of FITC-OVA endocytosis (<i>P</i> < 0.01) and surface MHC-II molecule expression (<i>P</i> < 0.01) in BMDCs, promoting promoted Treg cell differentiation. Mannose receptor (MR) knockdown significantly upregulated miR-223-3p, downregulated Rhob protein in OVA-treated DCs, inhibited the FITC-OVA endocytosis and surface MHC-II expression in BMDCs, and promoted Treg cell differentiation (all <i>P</i> < 0.01).<h4>Conclusion</h4>These data suggest that miR-223-3p has an inhibitory effect on the antigen uptake and presentation capacities of BMDCs and promotes Treg cell differentiation, which is, at least partially, through targeting MR signaling and Rhob."],"journal":["Journal of immunology research"],"pubmed_title":["miR-223-3p Inhibits Antigen Endocytosis and Presentation and Promotes the Tolerogenic Potential of Dendritic Cells through Targeting Mannose Receptor Signaling and Rhob."],"pmcid":["PMC7320286"],"funding_grant_id":["U0832007"],"pubmed_authors":["Zheng J","Tang HC","Lai YY","Xu G","Jiang HY"],"additional_accession":[]},"is_claimable":false,"name":"miR-223-3p Inhibits Antigen Endocytosis and Presentation and Promotes the Tolerogenic Potential of Dendritic Cells through Targeting Mannose Receptor Signaling and Rhob.","description":"<h4>Background</h4>The role of miR-223-3p in dendritic cells (DCs) is unknown. This study is aimed at investigating the effect of miR-223-3p on the antigen uptake and presentation capacities of DCs and the underlying molecular mechanism.<h4>Methods</h4>FITC-OVA antigen uptake and cell surface markers in bone marrow-derived DCs (BMDCs) were analyzed by flow cytometry. BMDCs were transfected with the miR-223-3p mimic or inhibitor. Cytokine levels were determined by ELISA. CD4+ T cell differentiation was determined by mixed lymphocyte culture assay.<h4>Results</h4>OVA treatment significantly downregulated miR-223-3p in BMDCs. The miR-223-3p mimic significantly inhibited OVA-induced antigen uptake and surface expression of MHC-II on BMDCs (<i>P</i> < 0.01). The miR-223-3p mimic increased TGF-<i>β</i>1 production in OVA-treated DCs (<i>P</i> < 0.01). Mixed lymphocyte reaction showed that the miR-223-3p mimic significantly promoted Treg cell differentiation. In addition, the miR-223-3p mimic significantly upregulated CD103 in DCs, indicating the promotion of tolerogenic DCs. The miR-223-3p mimic downregulated Rhob protein in OVA-induced DCs. Rhob knockdown significantly suppressed the ability of FITC-OVA endocytosis (<i>P</i> < 0.01) and surface MHC-II molecule expression (<i>P</i> < 0.01) in BMDCs, promoting promoted Treg cell differentiation. Mannose receptor (MR) knockdown significantly upregulated miR-223-3p, downregulated Rhob protein in OVA-treated DCs, inhibited the FITC-OVA endocytosis and surface MHC-II expression in BMDCs, and promoted Treg cell differentiation (all <i>P</i> < 0.01).<h4>Conclusion</h4>These data suggest that miR-223-3p has an inhibitory effect on the antigen uptake and presentation capacities of BMDCs and promotes Treg cell differentiation, which is, at least partially, through targeting MR signaling and Rhob.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020","modification":"2025-04-04T13:38:12.485Z","creation":"2020-11-20T08:54:12Z"},"accession":"S-EPMC7320286","cross_references":{"pubmed":["32656268"],"doi":["10.1155/2020/1379458"]}}