Endocytosis of commensal antigens by intestinal epithelial cells regulates mucosal T cell homeostasis.
basic_science · Level V
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- Record sourced from PubMed, PMID 30846568.
- Also identified by DOI 10.1126/science.aat4042 and PMC identifier 6708280.
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Abstract
Commensal bacteria influence host physiology, without invading host tissues. We show that proteins from segmented filamentous bacteria (SFB) are transferred into intestinal epithelial cells (IECs) through adhesion-directed endocytosis that is distinct from the clathrin-dependent endocytosis of invasive pathogens. This process transfers microbial cell wall-associated proteins, including an antigen that stimulates mucosal T helper 17 (T<sub>H</sub>17) cell differentiation, into the cytosol of IECs in a cell division control protein 42 homolog (CDC42)-dependent manner. Removal of CDC42 activity in vivo led to disruption of endocytosis induced by SFB and decreased epithelial antigen acquisition, with consequent loss of mucosal T<sub>H</sub>17 cells. Our findings demonstrate direct communication between a resident gut microbe and the host and show that under physiological conditions, IECs acquire antigens from commensal bacteria for generation of T cell responses to the resident microbiota.
Medical subject headings
- Antigens, Bacterial
- Endocytosis
- Gastrointestinal Microbiome
- Host Microbial Interactions
- Intestinal Mucosa
- Intraepithelial Lymphocytes
- Th17 Cells