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• W2419212529 abstract "Background It is becoming clear that platelets play a more significant role in the immune system than previously recognized 1-3 . Furthermore they are known to play a role in the induction of inflammation but the mechanisms by which they do so remain unclear. Both CLEC-2, which is highly expressed by platelets, and its ligand PDPN (gp38) are found in the joints of patients with rheumatoid arthritis (RA) 4 . However little is known about the role of CLEC-2-PDPN axis in synovial inflammation. Objectives To determine whether platelet-derived CLEC-2 induces synovial inflammation by triggering PDPN-expressing fibroblasts to adopt a pro-inflammatory phenotype. Methods Using flow cytometry we analyzed the PDPN expression in biopsies from RA patients as well as in mouse joints using the TNFΔare/+ and the anti-collagen antibodies induced arthritis (CAIA) models. We also induced arthritis in tamoxifen-induced CLEC-2 deficient mice to monitor the disease onset and resolution. After resolution, bones erosion and remodelling was assessed by micro-CT. We generated mouse PDPN Pos. and PDPN Neg. synovial fibroblasts (SF) that we co-cultured with wild-type or CLEC-2 deficient platelets. After incubation pro- and anti-inflammatory makers were measured at the mRNA (qPCR) and the protein (Luminex) levels. Results In human and mouse synovium, high levels of PDPN expression are found on SF as well as on a subset of haematopoietic cells. PDPN expression on mouse SF and myeloid cells is dynamic and depends on the level of inflammation. In vivo studies in which CLEC-2 is selectively deleted in platelets show that arthritis is more severe in absence of platelet-derived CLEC-2 suggesting that platelet-derived CLEC-2 plays a protective role in physiological conditions. However, in vitro co-culture data indicate that platelet-derived CLEC-2 induce SF to adopt a pro-inflammatory phenotype. This discrepancy between our in vitro and in vivo data might be explained by the fact that platelet-derived CLEC-2 induces myeloid cells to adopt an anti-inflammatory phenotype. Conclusions Our observations suggest that CLEC-2-PDPN interactions play a dual role in arthritis depending on whether they occur between platelets and fibroblasts or platelets and macrophages. References Benezech C, et al. CLEC-2 is required for development and maintenance of lymph nodes. Blood. 2014;123:3200-3207. Acton SE, et al. Dendritic cells control fibroblastic reticular network tension and lymph node. Nature. 2014;514:498-502 LID - 410.1038/nature13814 [doi]. Astarita JL, et al. The CLEC-2-podoplanin axis controls the contractility of fibroblastic reticular cells and lymph node microarchitecture. Nat Immunol. 2014:doi: 10.1038/ni.3035. Del Rey MJ, et al. Clinicopathological correlations of podoplanin (gp38) expression in rheumatoid synovium and its potential contribution to fibroblast platelet crosstalk. PLoS One. 2014;9:e99607. Disclosure of Interest None declared" @default.
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• W2419212529 date "2015-06-01" @default.
• W2419212529 modified "2023-09-23" @default.
• W2419212529 title "THU0035 A Key Role for Platelet-Derived Clec-2 in the Regulation of Synovial Inflammation" @default.
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• W2419212529 doi "https://doi.org/10.1136/annrheumdis-2015-eular.5533" @default.
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