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• W2884402012 abstract "Protease activated receptors (PARs) are a member of the G protein-activated receptor family and have been implicated in the pathogenesis of various disorders including autoimmune disease (e.g. PAR1 in IBD). These receptors are expressed multiple cell types including immune cells such as dendritic cells (DCs), a key immune regulator controlling the immune response. We have previously reported that PAR2 is expressed on dendritic cells and its activation suppressed antigen-specific CD4+ T cell priming. However, the role of PAR4 in modulating DC function is unclear. In the current study, we investigated the impact of PAR4 signalling in DCs. Bone marrow derived DCs were generated from the bone marrow of PAR4ko and WT mice. The expression of mannose receptor (MR) and the uptake capacity of FITC-conjugated dextran by PAR4ko DCs was assessed by flow cytometry. The expression of surface molecules on PAR4ko DCs and the production of cytokines by these DCs were analysed and compared to WT DCs before and after LPS stimulation. The contribution of PAR4 signalling to the capacity of these DCs to stimulate antigen-specific CD4+ T cell proliferation and cytokine production was investigated. We found that PARK4ko DCs expressed significantly lower levels of MR and had reduced capacity to uptake dextran compared to WT DCs. Following LPS stimulation, PAR4ko DCs expressed significantly lower levels of MHC class II as well as the accessary molecules CD80 and CD86, and produced less cytokines such as IL-12. There was no difference in the expression of surface molecules in DCs with no LPS treatment, suggesting cross talk of PAR4 and TLR4 signalling. In antigen-specific T cell activation experiments, pre-pulsed PAR4ko DCs with OVA peptide or OVA protein showed the reduced capacity to stimulate the proliferation of OT II CD4+ T cells and induce the production of cytokines such as IFNγ. These findings show that PAR4 signalling is required for DCs to develop their function, indicating the absence of PAR4 leads to the low immunogenicity of these DCs and a novel regulatory mechanism. Targeting of PAR4 has the potential to influence antigen-specific immune responses." @default.
• W2884402012 created "2018-08-03" @default.
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• W2884402012 date "2018-07-01" @default.
• W2884402012 modified "2023-09-26" @default.
• W2884402012 title "Modulation of Dendritic Cell Function by Protease Activated Receptor 4" @default.
• W2884402012 doi "https://doi.org/10.1097/01.tp.0000543653.45553.a1" @default.
• W2884402012 hasPublicationYear "2018" @default.
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