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- W4313356539 abstract "Abstract The development and proper functioning of the mammalian immune system relies on a reciprocal relationship between the host and the microbiota. These interactions shape both the composition of the microbiota along with the development and responsiveness of the immune system. Such a relationship requires mechanisms to reduce inflammatory immune responses within the intestine, which can damage the epithelial barrier and lead to the development of disorders such as inflammatory bowel disease. We find that CX3CR1 expressing mononuclear phagocytes (MNPs) are critical for maintaining this intestinal homeostasis. Using mice where we can selectively deplete CX3CR1+ MNPs in vivo, we demonstrate that CX3CR1+ MNPs in the lamina propria promote epithelial repair and, in models of colitis, limit TH1 responses against the microbiota itself. We also find they have functions in immune inductive sites such as the MLN where they limit the generation of inflammatory TH1 immune responses against pathogenic bacteria. Finally, we find they are required for the induction of antigen specific TH17 responses against members of the microbiota such as segmented filamentous bacteria (SFB). We find that the intact microbiota is critical for these homeostatic roles. After disruption of the microbiota with antibiotics, CX3CR1+ MNPs now promote inflammatory immune responses and are unable to promote epithelial barrier repair. Understanding this crucial relationship between the microbiota and intestinal immune cells will allow for selective targeting to modulate responsiveness of the intestinal immune system and promote homeostasis." @default.
- W4313356539 created "2023-01-06" @default.
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- W4313356539 date "2016-05-01" @default.
- W4313356539 modified "2023-10-16" @default.
- W4313356539 title "CX3CR1 mononuclear phagocytes utilize the microbiota to promote balanced intestinal immune responses" @default.
- W4313356539 doi "https://doi.org/10.4049/jimmunol.196.supp.136.7" @default.
- W4313356539 hasPublicationYear "2016" @default.
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