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- W2021090667 abstract "RATIONALE: We have shown that paramyxoviral respiratory infection induces expression of the high-affinity IgE receptor (FcεRI) on murine lung conventional dendritic cells (cDC). Cross-linking FcεRI results in CCL28 production, which recruits Th2 cells to the lung, and is associated with human and mouse models of asthma. We undertook this study to determine if other chemokines were produced upon cross-linking of cDC FcεRI. METHODS: C57BL6 mice were inoculated intranasally with 2x105 pfu Sendai virus. Five days post-inoculation mice were euthanized, lung cDCs were purified (>90%) by positive immunomagnetic bead selection, and FcεRI expression assessed by flow cytometry. cDCs were cultured with cross-linking anti-FcεRIα antibody (MAR-1) or control IgG for 6-30 h. After culture, mRNA was extracted from the cell pellets and analyzed for expression of CCL2 and CCL17 by real-time qRT-PCR, with data normalized to GAPDH mRNA levels. RESULTS: CCL2 expression was induced by FcεRI cross-linking at 6 and 30 hours (2.0±0.7 and 3.3±2 fold increase over IgG control, 6 and 30 hours, respectively, n=2). Similarly, CCL17 expression was also increased with FcεRI cross-linking (1.5±0.6 and 2.6±0.9 fold increase over IgG, 6 and 30 hours, respectively, n=2). CONCLUSIONS: Cross-linking FcεRI on lung cDC induces not only CCL28, but also message for CCL2 (a monocyte chemoattractant) and CCL17 (a Th2 cell chemoattractant associated with allergic disease). Whether these increases in message correlate with increased protein expression remains to be determined. Further studies will also explore the functional relevance of CCL2 and CCL17 in the paramyxoviral model of virus-induced atopic disease." @default.
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- W2021090667 date "2011-02-01" @default.
- W2021090667 modified "2023-09-27" @default.
- W2021090667 title "Cross-linking The High-affinity Receptor For IgE On Murine Lung Conventional Dendritic Cells Induces Ccl2 And Ccl17 Message Expression" @default.
- W2021090667 doi "https://doi.org/10.1016/j.jaci.2010.12.309" @default.
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