The immunology of mucosal models of inflammation.

By W. Strober, I. Fuss, R. Blumberg. Annual Review of Immunology, 2002

1,416 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/b72ccdf2aa4feca3b16deae55d3976dfcb3d94fc

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Herbert Tilg
2. Laurie H. Glimcher
3. H. Ishigame
4. Y. Iwakura
5. Ann-Hwee Lee
6. M. Lamkanfi
7. F. Powrie
8. Stefan Schreiber

In Genetics

1. H. Ishigame
2. Y. Iwakura
3. Andre Franke
4. M. Lamkanfi
5. F. Powrie
6. Stefan Schreiber
7. Laurie H. Glimcher
8. K. Boyd

In Immunology

1. Y. Iwakura
2. F. Powrie
3. H. Ishigame
4. M. Lamkanfi
5. T. Kanneganti
6. D. Cua
7. Laurie H. Glimcher
8. K. Maloy

Citations in the corpus

• The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis (2010, positive): “Excessive inflammatory and immune responses in the intestine are thought to be due to a breach in the epithelial barrier in the gut that segregates commensal microflora from the host’s systemic organs (Strober et al., 2002).”
• Current understanding of dysbiosis in disease in human and animal models (2016, background): “It has been suggested that an increased immune response toward the antigens of the dysbiotic gut microbiota may lead to this chronic, potentially CRC-causing inflammation.(47) Inflamm Bowel Dis Volume 22, Number 5, May 2016 Dysbiosis in Disease in Human and Animal Models”
• The Bile Acid Receptor FXR Is a Modulator of Intestinal Innate Immunity1 (2009, methodology): “The efficacy of INT-747 was tested in acute and chronic models of colon inflammation induced by trinitrobenzenesulfonic acid (TNBS) or dextran sulfate (DSS) (24, 25).”
• Interleukin-23 drives innate and T cell–mediated intestinal inflammation (2006, background): “Although the aetiopathogenesis of CD is not yet completely understood, it is widely held that chronic intestinal infl ammation is driven by the proinfl ammatory cytokine IL-12, which promotes the development of pathogenic Th1 CD4+ eff ector cells (3, 4).”
• Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis. (2004, neutral): “…the develop-ticularly macrophages, resident in the lamina propria of ment of intestinal epithelium, vasculature, and lymphoid the intestine (Strober et al., 2002) resulting in a potent tissue, and the contribution to the phenomena of…”
• XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease (2008, positive): “We therefore examined the in vivo effects of DSS, a toxin for mucosal epithelial cells that disrupts barrier function (Strober et al., 2002).”
• CD4+CD25+ TR Cells Suppress Innate Immune Pathology Through Cytokine-dependent Mechanisms (2003, background): “The key role that the immune system plays in regulating intestinal integrity has been demonstrated by the development of multiple rodent models of mucosal inflammation that are associated with immunological defects, particularly those that affect T cells (1).”
• Cutting Edge: Cure of Colitis by CD4+CD25+ Regulatory T Cells1 (2003, background): “Understanding of the pathogenesis of IBD has been aided by the development of animal models that mimic aspects of the human disease (2).”
• TLR Signaling in the Gut in Health and Disease1 (2005, background): “Animal models of IBD are generally characterized by a dominant Th1 phenotype (66).”