IL-23R+ innate lymphoid cells induce colitis via interleukin-22-dependent mechanism

[1]  G. Ho Faculty Opinions recommendation of Innate lymphoid cells drive interleukin-23-dependent innate intestinal pathology. , 2015 .

[2]  T. Kanai,et al.  RORγt-dependent IL-17A-producing cells in the pathogenesis of intestinal inflammation , 2012, Mucosal Immunology.

[3]  S. Levin,et al.  IL-17RE is the functional receptor for IL-17C and mediates mucosal immunity to infection with intestinal pathogens , 2011, Nature Immunology.

[4]  W. Ouyang,et al.  Opposing consequences of IL-23 signaling mediated by innate and adaptive cells in chemically induced colitis in mice , 2011, Mucosal Immunology.

[5]  E. Assier,et al.  Interleukin-23: A key cytokine in inflammatory diseases , 2011, Annals of medicine.

[6]  Peter J. Morrison,et al.  Interleukin‐23 and T helper 17‐type responses in intestinal inflammation: from cytokines to T‐cell plasticity , 2011, Immunology.

[7]  S. Travis,et al.  IL-23–responsive innate lymphoid cells are increased in inflammatory bowel disease , 2011, The Journal of experimental medicine.

[8]  Y. Wan,et al.  Memory/effector (CD45RBlo) CD4 T cells are controlled directly by IL-10 and cause IL-22–dependent intestinal pathology , 2011, The Journal of experimental medicine.

[9]  D. Artis,et al.  Border patrol: regulation of immunity, inflammation and tissue homeostasis at barrier surfaces by IL-22 , 2011, Nature Immunology.

[10]  D. Artis,et al.  CD4(+) lymphoid tissue-inducer cells promote innate immunity in the gut. , 2011, Immunity.

[11]  U. Pannicke,et al.  Regulated expression of nuclear receptor RORγt confers distinct functional fates to NK cell receptor-expressing RORγt(+) innate lymphocytes. , 2010, Immunity.

[12]  Todd Davidson,et al.  Generation of Pathogenic Th17 Cells in the Absence of TGF-β Signaling , 2010, Nature.

[13]  F. Powrie,et al.  Interleukin-23 Drives Intestinal Inflammation through Direct Activity on T Cells , 2010, Immunity.

[14]  D. Artis,et al.  Pathological versus protective functions of IL-22 in airway inflammation are regulated by IL-17A , 2010, The Journal of experimental medicine.

[15]  C. Hoggart,et al.  Pathway Analysis of GWAS Provides New Insights into Genetic Susceptibility to 3 Inflammatory Diseases , 2009, PloS one.

[16]  O. Boyman,et al.  Cutting Edge: IL-7 Regulates the Peripheral Pool of Adult RORγ+ Lymphoid Tissue Inducer Cells1 , 2009, The Journal of Immunology.

[17]  Richard A Flavell,et al.  A protective function for interleukin 17A in T cell–mediated intestinal inflammation , 2009, Nature Immunology.

[18]  V. Kuchroo,et al.  Cutting Edge: IL-23 Receptor GFP Reporter Mice Reveal Distinct Populations of IL-17-Producing Cells1 , 2009, The Journal of Immunology.

[19]  C. Tato,et al.  Lymphoid tissue inducer–like cells are an innate source of IL-17 and IL-22 , 2009, The Journal of experimental medicine.

[20]  A. Murphy,et al.  Innate and adaptive interleukin-22 protects mice from inflammatory bowel disease. , 2008, Immunity.

[21]  O. Mandelboim,et al.  Microbial flora drives interleukin 22 production in intestinal NKp46+ cells that provide innate mucosal immune defense. , 2008, Immunity.

[22]  T. Okanoue,et al.  Involvement of IL-17A in the pathogenesis of DSS-induced colitis in mice. , 2008, Biochemical and biophysical research communications.

[23]  E. Rickel,et al.  Identification of Functional Roles for Both IL-17RB and IL-17RA in Mediating IL-25-Induced Activities , 2008, The Journal of Immunology.

[24]  Judy H. Cho,et al.  Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease , 2008, Nature Genetics.

[25]  D. Fox,et al.  Th17 cells in human disease , 2008, Immunological reviews.

[26]  R. Broaddus,et al.  Regulation of inflammatory responses by IL-17F , 2008, The Journal of experimental medicine.

[27]  R. Xavier,et al.  IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis. , 2008, The Journal of clinical investigation.

[28]  A. Murphy,et al.  Interleukin-22 but not interleukin-17 provides protection to hepatocytes during acute liver inflammation. , 2007, Immunity.

[29]  D. Levy,et al.  IL-6 programs TH-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways , 2007, Nature Immunology.

[30]  Simon C. Potter,et al.  Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls , 2007, Nature.

[31]  P. Valdez,et al.  Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis , 2007, Nature.

[32]  Judy H. Cho,et al.  A Genome-Wide Association Study Identifies IL23R as an Inflammatory Bowel Disease Gene , 2006, Science.

[33]  F. Powrie,et al.  Interleukin-23 drives innate and T cell–mediated intestinal inflammation , 2006, The Journal of experimental medicine.

[34]  A. Sher,et al.  IL-23 plays a key role in Helicobacter hepaticus–induced T cell–dependent colitis , 2006, The Journal of experimental medicine.

[35]  L. Fouser,et al.  Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides , 2006, The Journal of experimental medicine.

[36]  M. Rojas,et al.  Selective Ablation of Matrix Metalloproteinase-2 Exacerbates Experimental Colitis: Contrasting Role of Gelatinases in the Pathogenesis of Colitis1 , 2006, The Journal of Immunology.

[37]  K. Toellner,et al.  Neonatal and Adult CD4+CD3− Cells Share Similar Gene Expression Profile, and Neonatal Cells Up-Regulate OX40 Ligand in Response to TL1A (TNFSF15)1 , 2006, The Journal of Immunology.

[38]  L. Hooper,et al.  Symbiotic Bacteria Direct Expression of an Intestinal Bactericidal Lectin , 2006, Science.

[39]  T. Mcclanahan,et al.  IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6. , 2006, The Journal of clinical investigation.

[40]  J. Kolls,et al.  Critical role of IL‐17 receptor signaling in acute TNBS‐induced colitis , 2006, Inflammatory bowel diseases.

[41]  W. Paul,et al.  Jak3 negatively regulates dendritic-cell cytokine production and survival. , 2005, Blood.

[42]  A. Takayanagi,et al.  Interleukin-22, a member of the IL-10 subfamily, induces inflammatory responses in colonic subepithelial myofibroblasts. , 2005, Gastroenterology.

[43]  T. Kirkegaard,et al.  Expression and localisation of matrix metalloproteinases and their natural inhibitors in fistulae of patients with Crohn’s disease , 2004, Gut.

[44]  C. Miao,et al.  High-level factor VIII gene expression in vivo achieved by nonviral liver-specific gene therapy vectors. , 2003, Human gene therapy.

[45]  T. Mcclanahan,et al.  A Receptor for the Heterodimeric Cytokine IL-23 Is Composed of IL-12Rβ1 and a Novel Cytokine Receptor Subunit, IL-23R1 , 2002, The Journal of Immunology.

[46]  R. Hershberg,et al.  Helicobacter-induced inflammatory bowel disease in IL-10- and T cell-deficient mice. , 2001, American journal of physiology. Gastrointestinal and liver physiology.

[47]  J Wagner,et al.  Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. , 2000, Immunity.

[48]  Thiennu H. Vu,et al.  Matrix metalloproteinases: effectors of development and normal physiology. , 2000, Genes & development.

[49]  C. J. Taylor,et al.  Matrix metalloproteinase levels are elevated in inflammatory bowel disease. , 1999, Gastroenterology.

[50]  R. Coffman,et al.  Phenotypically distinct subsets of CD4+ T cells induce or protect from chronic intestinal inflammation in C. B-17 scid mice. , 1993, International immunology.

[51]  B. Becher,et al.  RORgamma-expressing Th17 cells induce murine chronic intestinal inflammation via redundant effects of IL-17A and IL-17F. , 2009, Gastroenterology.