The IL-23/Th17 axis: therapeutic targets for autoimmune inflammation
- 1 December 2006
- journal article
- review article
- Published by Elsevier BV in Current Opinion in Immunology
- Vol. 18 (6), 670-675
- https://doi.org/10.1016/j.coi.2006.09.008
Abstract
No abstract availableKeywords
This publication has 51 references indexed in Scilit:
- A crucial role for interleukin (IL)-1 in the induction of IL-17–producing T cells that mediate autoimmune encephalomyelitisThe Journal of Experimental Medicine, 2006
- Selective regulatory function of Socs3 in the formation of IL-17-secreting T cellsProceedings of the National Academy of Sciences of the United States of America, 2006
- Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitisJCI Insight, 2006
- IL-23 is essential for T cell–mediated colitis and promotes inflammation via IL-17 and IL-6JCI Insight, 2006
- Transforming growth factor-β induces development of the TH17 lineageNature, 2006
- Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cellsNature, 2006
- Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineagesNature Immunology, 2005
- New IL-12-family members: IL-23 and IL-27, cytokines with divergent functionsNature Reviews Immunology, 2005
- Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brainNature, 2003
- Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses.JCI Insight, 1996