title: Disrupted regulatory T cell homeostasis in inflammatory bowel diseases.
abstract: In the gut, where billions of non-self-antigens from the food and the microbiota are present, the immune response must be tightly regulated to ensure both host protection against pathogenic microorganisms and the absence of immune-related pathologies. It has been well documented that regulatory T cells (Tregs) play a pivotal role in this context. Indeed, Tregs are able to prevent excessive inflammation, which can lead to the rupture of intestinal homeostasis observed in inflammatory bowel diseases (IBDs). Both the worldwide incidence and prevalence of such diseases have increased throughout the latter part of the 20(th) century. Therefore, it is crucial to understand how Tregs suppress the colitogenic immune cells to establish new treatments for patients suffering from IBDs. In this review, we will first summarize the results obtained in animal model studies that highlight the importance of Tregs in maintaining intestinal homeostasis and describe the specific suppressive mechanisms involved. Next, our current knowledge about Tregs contribution to human IBDs will be reviewed, as well as the current therapeutic perspective on using Tregs for clinical IBD treatment and the challenges that remain to be resolved to ensure both the safety and effectiveness of these therapies in targeting this critical immune-regulatory cell population.
authors.affiliation: Christophe Pedros, Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92307, United States.
authors.forename: Christophe
authors.initials: C
authors.lastname: Pedros
authors.affiliation: Christophe Pedros, Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92307, United States.
authors.forename: Fanny
authors.initials: F
authors.lastname: Duguet
authors.affiliation: Christophe Pedros, Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92307, United States.
authors.forename: Abdelhadi
authors.initials: A
authors.lastname: Saoudi
authors.affiliation: Christophe Pedros, Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92307, United States.
authors.forename: Marianne
authors.initials: M
authors.lastname: Chabod
mesh_terms: D000818:Animals; D005765:Gastrointestinal Agents / Q000627:therapeutic use; D000069196:Gastrointestinal Microbiome; D006706:Homeostasis; D054884:Host-Pathogen Interactions; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007167:Immunotherapy / Q000379:methods; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000628:therapy; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology; D010641:Phenotype; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology
chemical_list: D005765:Gastrointestinal Agents; D007166:Immunosuppressive Agents; D018836:Inflammation Mediators
keywords: Colitis; Foxp3; Gut; Inflammatory bowel disease; Regulatory T cells
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