Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation: Evidence in Crohn disease and experimental colitis in vivo

By R. Atreya, J. Mudter, S. Finotto, J. Müllberg, T. Jostock, S. Wirtz, M. Schütz, B. Bartsch, M. Holtmann, C. Becker and 13 more. Nature Medicine, 2000

1,336 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/8931af2cd771a8b927c9d0334276967d6eef9bb6

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Citations in the corpus

IL-6 signaling in autoimmunity, chronic inflammation and inflammation-associated cancer. (2011, background): “antibody caused significant suppression of colitis activity [8,89].”
Directing Transition from Innate to Acquired Immunity: Defining a Role for IL-61 (2005, background): “Indeed, blockade of sIL-6R signaling in experimental models of colitis prevents disease onset by suppressing Bcl-2 and Bcl-xL expression (30).”
A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “Then the IL-6/sIL-6R complex activates gp130-positive T cells lacking IL-6R, leading to the translocation of STAT-3 and subsequent activation of transcription of the antiapoptotic genes Bcl-2 and Bcl-xl [144].”
IL-6 and STAT3 are required for survival of intestinal epithelial cells and development of colitis associated cancer (2009, background): “In patients with inﬂammatory bowel disease (IBD), such as ulcerative colitis (UC), the risk of CRC development is much higher than in the general population (Langholz et al., 1992).”
Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “Previous reports have suggested that IL-6 is important for T cell survival in the context of inflammation (Atreya et al., 2000).”
IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6. (2006, background): “Blocking the IL-6 signaling pathway prevented the development of T cell–mediated murine colitis (16, 17).”
Probiotics and immunity (2009, background): “In addition, lamina propria T cells from IBD patients secrete elevated levels of IL-6, and IL-6/STAT-3 signaling is upregulated.(71,72) However, there are differences between the two clinical forms of IBD, with lamina propria T cells from CD patients showing Th1 polarization, whereas those of UC pat”
Il-6 and its soluble receptor orchestrate a temporal switch in the pattern of leukocyte recruitment seen during acute inflammation. (2001, methodology): “Similarly, to block sIL-6R-mediated responses in IL-6 / Cell surface expression of IL-6R was assessed by cytofluorometry mice, animals were intraperitoneally administered with human solu(FACScalibre; Becton Dickinson) using a monoclonal anti-human ble gp130 (250 ng/mouse; from R&D Systems), which ha”
Visfatin, an Adipocytokine with Proinflammatory and Immunomodulating Properties1 (2007, background): “in apoptosis resistance of lamina propria T cells (34).”
Targeting interleukin-6 in inflammatory autoimmune diseases and cancers. (2014, background): “In patients with IBD, trans-signaling of IL-6 can activate T cells in the lamina propria and up-regulate anti-apoptotic factors Bcl-2 and Bcl-xl (Atreya et al., 2000).”