title: Group 3 innate lymphoid cells: regulating host-commensal bacteria interactions in inflammation and cancer.
abstract: A delicate balance exists between the mammalian immune system and normally beneficial commensal bacteria that colonize the gastrointestinal tract, which is necessary to maintain tissue homeostasis. Dysregulation of these interactions between the host and commensal bacteria is causally associated with chronic inflammation and the development of cancer. In contrast, recent reports have highlighted that commensal bacteria also play an essential role in promoting anti-tumor immune responses in several contexts, highlighting a paradox whereby interactions between the host and commensal bacteria can influence both pro- and anti-tumor immunity. Given the critical roles for group 3 innate lymphoid cells (ILC3s) in regulating inflammation, tissue repair and host-microbe interactions in the intestine, here we discuss new evidence that ILC3s may profoundly influence the development, progression and control of tumors. In this review, we provide an overview of recent advances in understanding the impact of commensal bacteria on tumorigenesis, discuss recent findings identifying ILC3s as critical regulators of host-microbe interactions and highlight the emerging role of this immune cell population in cancer and their potential implication as a therapeutic target.
authors.affiliation: Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Department of Microbiology and Immunology and The Jill Robert's Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, 413 East 69th Street, Belfer Research Building 512, Box 190, New York, NY 10021, USA.
authors.forename: Jeremy
authors.initials: J
authors.lastname: Goc
authors.affiliation: Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Department of Microbiology and Immunology and The Jill Robert's Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, 413 East 69th Street, Belfer Research Building 512, Box 190, New York, NY 10021, USA.
authors.forename: Matthew R
authors.initials: MR
authors.lastname: Hepworth
authors.affiliation: Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Department of Microbiology and Immunology and The Jill Robert's Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, 413 East 69th Street, Belfer Research Building 512, Box 190, New York, NY 10021, USA gfsonnenberg@med.cornell.edu.
authors.forename: Gregory F
authors.initials: GF
authors.lastname: Sonnenberg
mesh_terms: D000818:Animals; D063646:Carcinogenesis; D006706:Homeostasis; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D007167:Immunotherapy; D007249:Inflammation / Q000276:immunology*; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology; D008214:Lymphocytes / Q000276:immunology* / Q000382:microbiology; D009369:Neoplasms / Q000276:immunology*; D013559:Symbiosis
keywords: cancer; commensal bacteria; innate lymphoid cells; intestinal homeostasis