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- W6635909 abstract "Abstract The lungs are constantly bombarded by inhaled antigen, both innocuous and harmful. In order to avoid a detrimental over-exuberant response to the myriad of harmless particles inhaled daily, the lung micro-environment is highly regulated. Alveolar macrophages are held in a state of tight suppression by CD200R, TGF-B and IL-10 signalling, and by the nuclear macrophage regulator PPAR-gamma. An absence of any of these immune modulators can severely impact on this tight macrophage regulation. When challenged with LPS in vitro, CD200R-/- alveolar macrophages produce higher levels of IL-6 and TNF compared to wild type controls; and an absence of PPAR-gamma in alveolar macrophages leads to Th1-associated pulmonary inflammation. Here we block IL-10R signalling at homeostasis using an IL-10R mAb and aim to investigate how this impacts on the phenotype of murine alveolar macrophages, whether they become more or less regulatory, classically or alternatively activated. Preliminary data suggests that an absence of IL-10R signalling affects the phenotype of alveolar macrophages at homeostasis. During a subsequent influenza infection and importantly, after IL-10R blockade has ceased, we see a heightened immune response in the IL-10R mAb-treated animals relative to controls. This indicates that even temporarily altering lung homeostasis can affect the outcome of a subsequent infection." @default.
- W6635909 created "2016-06-24" @default.
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- W6635909 date "2010-04-01" @default.
- W6635909 modified "2023-09-26" @default.
- W6635909 title "The effect of altering the homeostatic regulation of alveolar macrophages (48.7)" @default.
- W6635909 doi "https://doi.org/10.4049/jimmunol.184.supp.48.7" @default.
- W6635909 hasPublicationYear "2010" @default.
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