Interleukin 27 negatively regulates the development of interleukin 17–producing T helper cells during chronic inflammation of the central nervous system

By J. Stumhofer, A. Laurence, E. Wilson, Elaine Huang, C. Tato, Leanne M. Johnson, A. Villarino, Qiulong Huang, A. Yoshimura, D. Sehy and 5 more. Nature Immunology, 2006

1,042 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/1e9bad5044514deb8e2c82c221c9dbc5007139c0

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In Immunology

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Citations in the corpus

• The IL-23/Th17 axis in the immunopathogenesis of psoriasis. (2009, background): “Likewise, IL-27, belonging to the IL-6 family (Pflanz et al., 2002), also acts as a Th17 inhibitor, consistent with its capacity to drive a Th1 cell response (Batten et al., 2006; Stumhofer et al., 2006).”
• TGF-β and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain TH-17 cell–mediated pathology (2007, background): “IL-27 and IL-25, originally defined for their T H 1- and T H 2-promoting activities, also regulate T H -17 cell”
• TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1 (2007, result): “This viewpoint is in line with the finding that IL-27 inhibits T H 17 cells during chronic CNS inflammation through the action of SOCS3 (ref”
• Opposing regulation of the Il17 locus through direct, reciprocal actions of STAT3 and STAT5 (2011, background): “Cytokines such as interferon-γ (IFN-γ), IL-27 and IL-4 inhibit T H 17 differentiatio”
• Regulation of the immune response by the aryl hydrocarbon receptor (2018, background): “…sites may limit inflammation by Tr1-cell-independent mechanisms such as direct inhibitory effects on pathogenic Th17 cells (Batten et al., 2006; Rostami and Ciric, 2013; Stumhofer et al., 2006) and also indirect effects, for example by acting on recruited dendritic cells (Mascanfroni et al., 2013).”
• IL-6 in inflammation, immunity, and disease. (2014, background): “…and inhibited the activities of STAT1 or STAT5, which mediate the anti-inflammatory signals of IL-27 and IFNg, or IL-2, respectively (Harrington et al. 2005; Stumhofer et al. 2006; Laurence et al. 2007; Kimura et al. 2008), thus suppressing the inhibitory signals for the induction of Th17 cells.”
• IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia (2008, background): “Recently, it has been shown that IL-27 is a key negative regulator of T H 17 immunit”
• IL-17 family cytokines and the expanding diversity of effector T cell lineages. (2007, background): “In agreement with the findings of Hunter and colleagues (121), EAE induction was exacerbated in IL-27Rα-deficient mice and was associated with increased frequencies of Th17 cells in the CNS.”
• A dominant function for interleukin 27 in generating interleukin 10–producing anti-inflammatory T cells (2007, background): “Like IL-10, IL-27 is now considered an important anti-inflammatory cytokine, as it negatively regulates the generation of T H -17 cell”
• Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation. (2007, background): “Specifically, IL-4 (which primarily activates STAT6) and IFN-g and IL-27 (which activate STAT1) all inhibit IL-17 production (Batten et al., 2006; Harrington et al., 2005; Stumhofer et al., 2006).”