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- W4313386710 abstract "Abstract Rheumatoid Arthritis (RA) is a chronic inflammatory autoimmune disease whose etiology is unknown. Monocytes (Mo) and dendritic cells (DC) are major mediators of inflammation and immune regulation. We have previously shown that aza-bisphosphonate (ABP) dendrimer targets Mo and reduces inflammation and bone erosion in mouse arthritis. However, the potential effect of ABP on inflammatory human Mo and DC is not well understood. We have used ABP to treat human Mo and DC that were stimulated in vitro with the TLR4 agonist LPS and with IFN-γ. Mo were purified from PBMC collected from healthy blood donors. DC were obtained by 6-day culture of purified Mo in the presence of GM-CSF and IL-4. Mo and DC were then preincubated alone or with 10µM ABP dendrimer for 1h, followed by LPS and IFN-γ. We quantitated the production of pro-inflammatory cytokines and IL-10, as well as markers of DC activation and maturation. ABP significantly decreased the production of TNF-α, IL-12 and IL-23. Furthermore, treated DC exhibited a tolerogenic profile, as suggested by an increase in IL-10, decrease in IL-12, and inhibition of maturation as assessed by inhibition of the costimulatory molecules CD80 and CD86 and of CD83. Our data extend our previous observations on the anti-inflammatory properties of ABP on human Mo and demonstrate the induction of a tolerogenic profile on DC. These observations should elucidate the in vivo response of the monocytic lineage to ABP as a novel compound for arthritis." @default.
- W4313386710 created "2023-01-06" @default.
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- W4313386710 date "2013-05-01" @default.
- W4313386710 modified "2023-10-18" @default.
- W4313386710 title "Activation of monocytes and dendritic cells through TLR4: modulation by dendrimer ABP as a potential therapeutic agent. (P5226)" @default.
- W4313386710 doi "https://doi.org/10.4049/jimmunol.190.supp.67.9" @default.
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