Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17–producing T cells

By M. Batten, Ji Li, S. Yi, Noelyn M. Kljavin, D. Danilenko, S. Lucas, James M. Lee, F. J. Sauvage, N. Ghilardi. Nature Immunology, 2006

910 citations recorded by the source corpus.

Subfields: Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/a0f79ad16c37cfebd22d05dcfd12d0afb79db0dc

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In Immunology

1. D. Cua
2. A. Jetten
3. C. Dong
4. Dan R. Littman
5. V. Kuchroo
6. R. Flavell
7. C. Weaver
8. W. E. Paul

In Pathology and Forensic Medicine

1. D. Cua
2. Dan R. Littman
3. V. Kuchroo
4. C. Weaver
5. Y. Iwakura
6. E. Bettelli
7. L. Harrington
8. Paul R. Mangan

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).”
• Plasticity of CD4+ T cell lineage differentiation. (2009, background): “…IL-27, a member of the heterodimeric IL-12 cytokine family, promotes Th1 cell differentiation by inducing T-bet and IL-12Rb2 (Takeda et al., 2003; Lucas et al., 2003) and concurrently inhibits Th17 cell differentiation in a Stat1-dependent manner (Batten et al., 2006; Stumhofer et al., 2006).”
• IL‐35 is a novel cytokine with therapeutic effects against collagen‐induced arthritis through the expansion of regulatory T cells and suppression of Th17 cells (2007, result): “In contrast, other studies demonstrated that IL-27 was an antagonist of Th17 cell activity [ 27 , 28].”
• Discovery and biology of IL-23 and IL-27: related but functionally distinct regulators of inflammation. (2007, background): “However, as discussed below, other studies with EAE have found that IL-27R knockout (KO) mice are more susceptible to disease (52), and initial reports with p28 note that it did not stimulate significant T cell proliferation or IFN-γ production (4).”
• Interleukins (from IL-1 to IL-38), interferons, transforming growth factor β, and TNF-α: Receptors, functions, and roles in diseases. (2016, background): “124 It directly antagonizes the development of TH17 cell responses and limits the induction of inflammation by cells that produce IL-17 in the central nervous system.(125) IL-27 also limits the development of uveitis and scleritis by cells that produce IL-17 and induces FOXP3 expression by Treg cell”
• TH-17 cells in the circle of immunity and autoimmunity (2007, background): “The absence of IL-27-mediated signaling exacerbates neuroinflammation, enhances the generation of T H -17 cells and increases the number of IL-17-expressing T cells in inflamed tissu”
• 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”
• Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells. (2008, background): “, 2006), whereas IL-25, IL-27, and T-bet may be negative regulators of IL-17 production (Batten et al., 2006; Rangachari et al., 2006; Stumhofer et al., 2006; Kleinschek et al., 2007).”
• IL-6 programs TH-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways (2007, background): “Among these, IL-2 and IL-27 strongly inhibit specification of the T H -17 lineag”
• A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell–mediated tissue damage (2007, result): “This was demonstrated in two studies where defective IL-27 signaling led to a predicted increase in inflammation in the brain resulting from either EAE (refs”