Induction of intestinal Th17 cells by segmented filamentous bacteria

By I. Ivanov, K. Atarashi, N. Manel, Eoin L. Brodie, T. Shima, U. Karaoz, D. Wei, Katherine C. Goldfarb, C. Santee, S. Lynch and 7 more. Cell, 2009

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SUMMARY The gastrointestinal tract of mammals is inhabited by hundreds of distinct species of commensal microorganisms that exist in a mutualistic relationship with the host. How commensal microbiota influence the host immune system is poorly understood. We show here that colonization of the small intestine of mice with a single commensal microbe, segmented filamentous bacterium (SFB), is sufficient to induce the appearance of CD4+ T helper cells that produce IL-17 and IL-22 (Th17 cells) in the lamina propria. SFB adhere tightly to the surface of epithelial cells in the terminal ileum of mice with Th17 cells but are absent from mice that have few Th17 cells. Colonization with SFB was correlated with increased expression of genes associated with inflammation and anti-microbial defenses, and resulted in enhanced resistance to the intestinal pathogen Citrobacter rodentium. Thus, manipulation of this commensalregulated pathway may provide new opportunities for enhancing mucosal immunity and treating autoimmune disease.

Subfields: Genetics, Infectious Diseases, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7e48b69cdf8cf5d02fe1998e206523d85e21130e

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Citations in the corpus

Individual intestinal symbionts induce a distinct population of RORγ+ regulatory T cells (2015, background): “Segmented Filamentous Bacteria (SFB), classic inducers of Rorγ-dependent Th17 cells (20) and which elicit IL17-producing Tregs in the small intestine (SI) (21), were only mediocre inducers of colonic Rorγ+ Tregs, reinforcing the distinction between the cell populations.”
Gut Microbiota and Immune System Interactions (2020, background): “In germ-free murine models, T-cell subsets in the gut are abnormal, displaying reduced responses of Th17 in the lamina propria of the small intestine and Treg in the colonic lamina propria [133,134].”
Microbiota-Dependent Crosstalk Between Macrophages and ILC3 Promotes Intestinal Homeostasis (2014, positive): “Accumulated evidence suggests that gut commensals contribute to the maintenance of intestinal homeostasis, partly through their ability to control the differentiation of effector T lymphocytes in the mucosa (3, 4) and to modulate inflammatory responses through the induction of Tregs and interleukin-”
Early life antibiotic‐driven changes in microbiota enhance susceptibility to allergic asthma (2012, neutral): “For example, Bacteroides fragilis modulates T-helpertype 1/2 (Th1/Th2) balance [16], segmented filamentous bacteria direct Th17 cell differentiation [17] and Clostridium species induce regulatory T-cell (Treg) production [18].”
Ly6C hi monocytes in the inflamed colon give rise to proinflammatory effector cells and migratory antigen-presenting cells. (2012, background): “, the prevalence of distinct helper and regulatory T cell populations (Atarashi et al., 2011; Ivanov et al., 2009).”
The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells (2011, background): “…cells in the small intestine can be promoted by specific commensal gut flora (e.g., segmented filamentous bacteria) (Gaboriau-Routhiau et al., 2009; Ivanov et al., 2009), it is still under debate whether the development of NK-22 cells requires intestinal symbionts (Reynders et al., 2011; Sanos et…”
Human nutrition, the gut microbiome, and immune system: envisioning the future (2011, background): “— a member of the Clostridiaceae family that drives intestinal T H 17 responses in mic”
Tryptophan catabolites from microbiota engage aryl hydrocarbon receptor and balance mucosal reactivity via interleukin-22. (2013, positive): “In mice, autochthonous SFB are responsible for Th17 accumulation and IL-22 production by Th17 cells in the gut (Ivanov et al., 2009), but it has been unclear whether and which signals from the microbiota selectively direct the production of IL-22 by ILC3s (Lee et al., 2012).”
Commensal Bacteria Calibrate the Activation Threshold of Innate Antiviral Immunity (2012, background): “Conversely, commensal bacteria can also boost immune responses against mucosal infections (Benson et al., 2009; Hall et al., 2008; Ichinohe et al., 2011; Ivanov et al., 2009).”
Microbiota-modulated metabolites shape the intestinal microenvironment by regulating NLRP6 inflammasome signaling (2015, background): “Remarkably, disease-promoting dysbiotic microbiota in multiple mouse models harbors dominance, upon fecal transfer, over a previously stable wild-type (WT) microbiota, leading to transferable disease susceptibility (Couturier-Maillard et al., 2013; Elinav et al., 2011; Garrett et al., 2007; Henao-Me”