Interleukin-6: from basic science to medicine--40 years in immunology.
By T. Kishimoto. Annual Review of Immunology, 2005
1,067 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/71568f66e3a1862dcee61e897048dd20ece6d61f
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Citations in the corpus
- IL-6 Trans-Signaling via the Soluble IL-6 Receptor: Importance for the Pro-Inflammatory Activities of IL-6 (2012, background): “Since all cells in the body express gp130 [9, 10], theoretically, all cells can be activated by the IL-6/sIL-6R complex.”
- Tumor self-seeding by circulating cancer cells (2009, methodology): “of immune and inflammatory responses and have been implicated in tumor progression (Hodge et al., 2005; Kishimoto, 2005).”
- Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas. (2007, background): “The IL-6 family cytokines, including IL-6, OSM, and LIF, share the same gp130signaling receptor, leading to activation of JAK1, JAK2, and Tyk2 and subsequent phosphorylation of STAT3 (21, 23).”
- Interleukin-6 in aging and chronic disease: a magnificent pathway. (2006, background): “Cardiac myxoma, a benign atrial heart tumor, produces large quantities of IL-6, which cause autoantibody production, fever, joint pain, and anemia (108).”
- IL-6 and STAT3 are required for survival of intestinal epithelial cells and development of colitis associated cancer (2009, background): “By binding to its gp130-associated receptor, IL-6 activates three separate signaling pathways, namely Shp2-Ras-ERK, JAK1/2-Stat3, and PI3K-Akt-mTOR (Kishimoto, 2005).”
- IL-17 and Th17 Cells. (2009, background): “Depending on the cellular source of IL-6, cytokines such as IL-1, tumor necrosis factor (TNF), plateletderived growth factor (PDGF), IL-3, GMCSF, and IL-17 are important inducers of IL-6 (39, 40).”
- Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy. (2008, background): “Interleukin-6 (IL-6) is a pleiotropic cytokine associated with the control and coordination of immune responses (Kishimoto, 2005).”
- Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis (2011, methodology): “Peripheral T cell blasts from a patient displayed normal STAT3 activation in response to IL-23, as shown by WB (Fig.”
- Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype (2010, background): “IL-6 is a potent activator of megakaryocyte survival, differentiation and platelet formatio”
- IL-6 in inflammation, immunity, and disease. (2014, neutral): “5) (Kishimoto 2005).”