title: Immunopathology of inflammatory bowel disease.
abstract: Inflammatory bowel disease (IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system. The host microbiome, as well as viruses and fungi, play important roles in the development of IBD either by causing inflammation directly or indirectly through an altered immune system. New technologies have allowed researchers to be able to quantify the various components of the microbiome, which will allow for future developments in the etiology of IBD. Various components of the mucosal immune system are implicated in the pathogenesis of IBD and include intestinal epithelial cells, innate lymphoid cells, cells of the innate (macrophages/monocytes, neutrophils, and dendritic cells) and adaptive (T-cells and B-cells) immune system, and their secreted mediators (cytokines and chemokines). Either a mucosal susceptibility or defect in sampling of gut luminal antigen, possibly through the process of autophagy, leads to activation of innate immune response that may be mediated by enhanced toll-like receptor activity. The antigen presenting cells then mediate the differentiation of naïve T-cells into effector T helper (Th) cells, including Th1, Th2, and Th17, which alter gut homeostasis and lead to IBD. In this review, the effects of these components in the immunopathogenesis of IBD will be discussed.
authors.affiliation: Kori L Wallace, Yoshitake Kanazawa, David Q Shih, F Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles CA 90048, United States.
authors.forename: Kori L
authors.initials: KL
authors.lastname: Wallace
authors.affiliation: Kori L Wallace, Yoshitake Kanazawa, David Q Shih, F Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles CA 90048, United States.
authors.forename: Li-Bo
authors.initials: LB
authors.lastname: Zheng
authors.affiliation: Kori L Wallace, Yoshitake Kanazawa, David Q Shih, F Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles CA 90048, United States.
authors.forename: Yoshitake
authors.initials: Y
authors.lastname: Kanazawa
authors.affiliation: Kori L Wallace, Yoshitake Kanazawa, David Q Shih, F Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles CA 90048, United States.
authors.forename: David Q
authors.initials: DQ
authors.lastname: Shih
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D001343:Autophagy; D001419:Bacteria / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D018928:Immunity, Mucosal; D018836:Inflammation Mediators / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D007422:Intestines / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D064307:Microbiota; D012307:Risk Factors; D015398:Signal Transduction; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology
chemical_list: D018836:Inflammation Mediators
keywords: Adaptive immune system; Autophagy; Crohn’s disease; Inflammatory bowel disease; Innate immune system; Innate lymphoid cells; Microbiome; T helper 17; TL1A; Ulcerative colitis