Increased expression of interleukin 17 in inflammatory bowel disease

By Sanae Fujino, A. Andoh, S. Bamba, A. Ogaẃa, K. Hata, Y. Araki, T. Bamba, Y. Fujiyama. Gut, 2003

1,773 citations recorded by the source corpus.

Subfields: Genetics, Immunology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/7d281a3b4e35f1e30f027df428b6146b1ea38f59

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In Genetics

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In Immunology

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Citations in the corpus

• IL-23–responsive innate lymphoid cells are increased in inflammatory bowel disease (2011, background): “…(Wilson et al., 2007) are elevated in the intestine and serum of patients with IBD, and Th17 cells with an activated phenotype are present in the colon and blood of patients with Crohn’s disease (CD; Fujino et al., 2003; Andoh et al., 2005; Di Sabatino et al., 2009; Kleinschek et al., 2009).”
• The biological functions of T helper 17 cell effector cytokines in inflammation. (2008, neutral): “Specifically, this is true in the colonic mucosa of patients with either ulcerative colitis or Crohn's disease, when compared with corresponding samples from normal subjects or patients with infectious or ischemic colitis (Fujino et al., 2003).”
• Interleukin-22 but not interleukin-17 provides protection to hepatocytes during acute liver inflammation. (2007, background): “…and IL-22 are upregulated in the lesions of patients with various chronic inflammatory diseases, such as psoriasis, inflammatory bowel disease, and rheumatoid arthritis (Andoh et al., 2005; Chabaud et al., 1998; Fujino et al., 2003; Liang et al., 2006; Teunissen et al., 1998; Wolk et al., 2004).”
• Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17–producing human T helper cells (2007, background): “In humans, several studies have demonstrated a correlation between the severity of inflammatory disease and IL-17 concentrations in serum or tissue”
• Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “Furthermore, phosphorylated STAT3 and IL-17 are features of the inflammatory response in IBDs and colitis models, but the requirement for STAT3 in models of colitis, particularly with respect to T cell-dependent pathology, has not been explored (Fujino et al., 2003; Suzuki et al., 2001).”
• A protective function for interleukin 17A in T cell–mediated intestinal inflammation (2009, neutral): “In addition, there is higher expression of IFN-γ and IL-17 in the intestinal mucosa of patients with Crohn's diseas”
• Chronic Inflammation and Cytokines in the Tumor Microenvironment (2014, background): “Other inflammatory mediators are also involved, such as the proinflammatory cytokine IL-17, which was found to be elevated in the mucosa and serum of active IBD patients [203].”
• Innate and adaptive interleukin-22 protects mice from inflammatory bowel disease (2008, background): “Each dot represents one mouse; the bar indicates the mean; ND = not detected. like IL-22, is upregulated during chronic inflammatory diseases such as IBD, rheumatoid arthritis, and psoriasis (Laan et al., 1999; Liang et al., 2006) (Fujino et al., 2003; Kotake et al., 1999).”
• IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6. (2006, background): “org Volume 116 Number 5 May 2006 1313 Heightened IL-6 (19) and IL-17 levels (20) could be detected in both serum and intestinal tissue from patients with Crohn disease.”
• A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “Studies have shown that large amounts of IL-17-producing cells are mainly accumulated in the lamina propria of ulcerative colitis patients and in the submucosa and muscularis propria of Crohn’s disease patients [163].”
• Mechanisms of Disease: pathogenesis of Crohn's disease and ulcerative colitis (2006, background): “The levels of both IL-23 and IL-17 are increased in Crohn's disease tissues and most forms of experimental colitis”