A rush to judgment on Th17
Open Access
- 30 June 2008
- journal article
- editorial
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 205 (7), 1517-1522
- https://doi.org/10.1084/jem.20072066
Abstract
Some immunologists have characterized T helper (Th)17 T cells as the master mediators of tissue damage in a variety of pathological conditions. New data now demonstrate that Th1 and Th17 T cells are independently capable of inducing disease in two established models of autoimmunity. Thus, the role of Th17 cytokines as the central mediators of pathological tissue damage seems to require clarification.Keywords
This publication has 50 references indexed in Scilit:
- IL-21 and TGF-β are required for differentiation of human TH17 cellsNature, 2008
- Interleukin 10 suppresses Th17 cytokines secreted by macrophages and T cellsEuropean Journal of Immunology, 2008
- Alternative translation of osteopontin generates intracellular and secreted isoforms that mediate distinct biological activities in dendritic cellsProceedings of the National Academy of Sciences of the United States of America, 2008
- The differentiation of human TH-17 cells requires transforming growth factor-β and induction of the nuclear receptor RORγtNature Immunology, 2008
- Differential regulation of central nervous system autoimmunity by TH1 and TH17 cellsNature Medicine, 2008
- Development, cytokine profile and function of human interleukin 17–producing helper T cellsNature Immunology, 2007
- Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17–producing human T helper cellsNature Immunology, 2007
- TH-17 cells in the circle of immunity and autoimmunityNature Immunology, 2007
- Interleukin-23 drives innate and T cell–mediated intestinal inflammationThe Journal of Experimental Medicine, 2006
- IL-23 plays a key role inHelicobacter hepaticus–induced T cell–dependent colitisThe Journal of Experimental Medicine, 2006