Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis.

By Yi Chen, C. Langrish, Brent S. McKenzie, B. Joyce-Shaikh, J. Stumhofer, T. Mcclanahan, W. Blumenschein, Tatyana Churakovsa, Justin T. Low, L. Presta and 3 more. Journal of Clinical Investigation, 2006

626 citations recorded by the source corpus.

Subfields: Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/c7cc78f6d796a2386ca23fd88ab411a954a61125

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Citations in the corpus

The adaptor Act1 is required for interleukin 17–dependent signaling associated with autoimmune and inflammatory disease (2007, background): “In addition, Act1-deficient mice on a C57BL/6 (B6) background had much less myelin oligodendrocyte glycoprotein (MOG)–induced EAE and dextran sodium sulfate (DSS)–induced colitis, both of which are IL-17-dependent inflammatory disease”
Interleukin-23 drives innate and T cell–mediated intestinal inflammation (2006, methodology): “was produced and characterized as previously described (56).”
Interleukin 27 negatively regulates the development of interleukin 17–producing T helper cells during chronic inflammation of the central nervous system (2006, background): “These 'T H -17' lymphocytes have been suggested to be mediators of the inflammation associated with several autoimmune diseases, including experimental autoimmune encephalitis (EAE) and collagen-induced arthriti”
A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell–mediated tissue damage (2007, background): “Likewise, mice treated with antibodies to IL-23 failed to develop EAE (ref”
IL-17 family cytokines and the expanding diversity of effector T cell lineages. (2007, background): “Additional studies correlated the expression of RORγt with Th17 development and immunopathology in a model of EAE and demonstrated that IL6-deficient mice showed a correlative loss of Th17 and RORγt+ intestinal lymphocytes.”
Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis. (2008, background): “EAE severity was also greatly reduced on treatment with a monoclonal antibody to IL-17(3); similarly, mice treated with an antibody against IL-23 failed to develop EAE.(7) Although EAE could still occur in IL-17 knockout mice, the disease was heavily attenuated,(8) and mice deficient for the key tra”
Epigenetic control of T-helper-cell differentiation (2009, result): “There is some evidence in support of the contrary, which shows that T-bet, IFNγ, RORγt and IL-17 are often co-expressed by cells in vivo and that T-bet may help to induce the expression of IL-23R and be induced by IL-23 in T H 17 cell”