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Ladinsky, Mark S; Araujo, Leandro P; Zhang, Xiao; Veltri, John; Galan-Diez, Marta; Soualhi, Salima; Lee, Carolyn; Irie, Koichiro; Pinker, Elisha Y; Narushima, Seiko; Bandyopadhyay, Sheila; Nagayama, Manabu; Elhenawy, Wael; Coombes, Brian K; Ferraris, Ronaldo P; Honda, Kenya; Iliev, Iliyan D; Gao, Nan; Bjorkman, Pamela J; Ivanov, Ivaylo I
Science (American Association for the Advancement of Science), 03/2019, Letnik: 363, Številka: 6431Journal Article
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 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 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.
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