APC-derived cytokines and T cell polarization in autoimmune inflammation
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Open Access
- 1 May 2007
- journal article
- review article
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 117 (5) , 1119-1127
- https://doi.org/10.1172/jci31720
Abstract
T cell–mediated autoimmune diseases such as multiple sclerosis and rheumatoid arthritis are driven by autoaggressive Th cells. The pathogenicity of such Th cells has, in the past, been considered to be dictated by their cytokine polarization profile. The polarization of such effector T cells relies critically upon the actions of cytokines secreted by APCs. While Th1 polarization has long been associated with the pathogenesis of autoimmune diseases, recent data obtained in gene-targeted mice and the discovery of Th17 cell involvement in autoimmunity conflict with this hypothesis. In light of these recent developments, we discuss in this review the actions of APC-derived cytokines and their emerging roles in T cell polarization in the context of autoimmune inflammatory responses.Keywords
This publication has 121 references indexed in Scilit:
- T cell self-reactivity forms a cytokine milieu for spontaneous development of IL-17+ Th cells that cause autoimmune arthritisThe Journal of Experimental Medicine, 2007
- IL-25 regulates Th17 function in autoimmune inflammationThe Journal of Experimental Medicine, 2007
- Responses of IL-18- and IL-18 receptor-deficient pancreatic islets with convergence of positive and negative signals for the IL-18 receptorProceedings of the National Academy of Sciences, 2006
- Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destructionThe Journal of Experimental Medicine, 2006
- Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptidesThe Journal of Experimental Medicine, 2006
- 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
- T‐bet is essential for the progression of experimental autoimmune encephalomyelitisImmunology, 2006
- Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitisJournal of Clinical Investigation, 2006
- Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cellsNature, 2006
- Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brainNature, 2003