Opposing consequences of IL-23 signaling mediated by innate and adaptive cells in chemically induced colitis in mice.
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Murine models of inflammatory bowel disease (IBD): challenges of modeling human diseaseMulti-scale in vivo systems analysis reveals the influence of immune cells on TNF-α-induced apoptosis in the intestinal epitheliumCytokines, IBD, and colitis-associated cancerEpithelial IL-23R Signaling Licenses Protective IL-22 Responses in Intestinal InflammationNod/Ripk2 signaling in dendritic cells activates IL-17A-secreting innate lymphoid cells and drives colitis in T-bet-/-.Rag2-/- (TRUC) mice.The necroptosis adaptor RIPK3 promotes injury-induced cytokine expression and tissue repair.Preclinical development of AMG 139, a human antibody specifically targeting IL-23The dichotomous pattern of IL-12r and IL-23R expression elucidates the role of IL-12 and IL-23 in inflammation.Lymphotoxin beta receptor signaling limits mucosal damage through driving IL-23 production by epithelial cells.Interleukin-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability.Intestinal Epithelial Cell Tyrosine Kinase 2 Transduces IL-22 Signals To Protect from Acute Colitis.Increased Expression of DUOX2 Is an Epithelial Response to Mucosal Dysbiosis Required for Immune Homeostasis in Mouse IntestineInflammation and colorectal cancer: colitis-associated neoplasia.Diversity, function, and transcriptional regulation of gut innate lymphocytesDeletion of cationic amino acid transporter 2 exacerbates dextran sulfate sodium colitis and leads to an IL-17-predominant T cell responseExpression of the novel adipokine C1qTNF-related protein 4 (CTRP4) suppresses colitis and colitis-associated colorectal cancer in mice.IL-23R+ innate lymphoid cells induce colitis via interleukin-22-dependent mechanism.The Th17 pathway and inflammatory diseases of the intestines, lungs, and skinHealing of intestinal inflammation by IL-22.IL-22 in tissue-protective therapy.Targeting interleukins for the treatment of inflammatory bowel disease-what lies beyond anti-TNF therapy?Interleukin 23 in Crohn's disease.Interleukin-23 is sufficient to induce rapid de novo gut tumorigenesis, independent of carcinogens, through activation of innate lymphoid cells.Innate lymphoid cells in intestinal immunity and inflammation.Though Active on RINm5F Insulinoma Cells and Cultured Pancreatic Islets, Recombinant IL-22 Fails to Modulate Cytotoxicity and Disease in a Protocol of Streptozotocin-Induced Experimental DiabetesLessons Learned From Trials Targeting Cytokine Pathways in Patients With Inflammatory Bowel Diseases.IgA-coated E. coli enriched in Crohn's disease spondyloarthritis promote TH17-dependent inflammation.Cytokines IL-17 and IL-22 in the host response to infection.Postbiotic Modulation of Retinoic Acid Imprinted Mucosal-like Dendritic Cells by Probiotic Lactobacillus reuteri 17938 In Vitro.Role of interferon-γ and inflammatory monocytes in driving colonic inflammation during acute Clostridium difficile infection in mice.HMGB1 exacerbates experimental mouse colitis by enhancing innate lymphoid cells 3 inflammatory responses via promoted IL-23 production.β-Arrestin-1 deficiency protects mice from experimental colitis.An entirely automated method to score DSS-induced colitis in mice by digital image analysis of pathology slides.Interleukin-23 (IL-23), independent of IL-17 and IL-22, drives neutrophil recruitment and innate inflammation during Clostridium difficile colitis in mice.IL-23 activates innate lymphoid cells to promote neonatal intestinal pathology.Enteric mucosa integrity in the presence of a preserved innate interleukin 22 compartment in HIV type 1-treated individuals.Anti-inflammatory natural product goniothalamin reduces colitis-associated and sporadic colorectal tumorigenesis.Knockdown of myeloid cell hypoxia-inducible factor-1α ameliorates the acute pathology in DSS-induced colitis.Innate Lymphoid Cells in HIV/SIV Infections.Clinical importance of IL-22 cascade in IBD.
P2860
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P2860
Opposing consequences of IL-23 signaling mediated by innate and adaptive cells in chemically induced colitis in mice.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年学术文章
@wuu
2011年学术文章
@zh
2011年学术文章
@zh-cn
2011年学术文章
@zh-hans
2011年学术文章
@zh-my
2011年学术文章
@zh-sg
2011年學術文章
@yue
2011年學術文章
@zh-hant
name
Opposing consequences of IL-23 ...... cally induced colitis in mice.
@en
Opposing consequences of IL-23 ...... cally induced colitis in mice.
@nl
type
label
Opposing consequences of IL-23 ...... cally induced colitis in mice.
@en
Opposing consequences of IL-23 ...... cally induced colitis in mice.
@nl
prefLabel
Opposing consequences of IL-23 ...... cally induced colitis in mice.
@en
Opposing consequences of IL-23 ...... cally induced colitis in mice.
@nl
P2093
P2860
P356
P1433
P1476
Opposing consequences of IL-23 ...... ically induced colitis in mice
@en
P2093
P2860
P2888
P304
P356
10.1038/MI.2011.54
P577
2011-11-16T00:00:00Z