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• W3039223589 startingPage "102508" @default.
• W3039223589 abstract "Priming of autoreactive T cells in lymph nodes by dendritic cells (DCs) is critical for the pathogenesis of experimental autoimmune encephalitis (EAE). DC activation reflects a balance of pro- and anti-inflammatory signals. One anti-inflammatory factor is prostaglandin D2 signaling through its cognate receptor, D-prostanoid receptor 1 (PTGDR), on myeloid cells. Loss of PTGDR signaling might be expected to enhance DC activation and EAE but here we show that PTGDR−/− mice developed only mild signs of MOG35-55 peptide immunization-induced EAE. Compared to wild type mice, PTGDR−/− mice exhibited less demyelination, decreased leukocyte infiltration and diminished microglia activation. These effects resulted from increased pro-inflammatory responses in the lymph nodes, most notably in IL-1β production, with the unexpected consequence of increased activation-induced apoptosis of MOG35-55 peptide-specific T cells. Conditional deletion of PTGDR on DCs, and not other myeloid cells ameliorated EAE. Together, these results demonstrate the indispensable role that PGD2/PTGDR signaling on DCs has in development of pathogenic T cells in autoimmune demyelination." @default.
• W3039223589 created "2020-07-10" @default.
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• W3039223589 date "2020-11-01" @default.
• W3039223589 modified "2023-09-27" @default.
• W3039223589 title "Prostaglandin D2 signaling in dendritic cells is critical for the development of EAE" @default.
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• W3039223589 doi "https://doi.org/10.1016/j.jaut.2020.102508" @default.
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