*Current address: Department of Cell biology and Histology, Amsterdan Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited
Article first published online: 30 OCT 2008
© 2008 Schering Corporation. Journal compilation © 2008 Blackwell Munksgaard
Special Issue: New Paradigms in Inflammation
Volume 226, Issue 1, pages 132–146, December 2008
How to Cite
Boniface, K., Blom, B., Liu, Y.-J. and De Waal Malefyt, R. (2008), From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited. Immunological Reviews, 226: 132–146. doi: 10.1111/j.1600-065X.2008.00714.x
- Issue published online: 30 OCT 2008
- Article first published online: 30 OCT 2008
- Th17 cells;
Summary: Protracted inflammation leading to dysregulation of effector T-cell responses represents a common feature of a wide range of autoimmune diseases. The interleukin-12 (IL-12)/T-helper 1 (Th1) pathway was thought to be responsible for the pathogenesis of multiple chronic inflammatory diseases, including psoriasis, inflammatory bowel disease, arthritis, or multiple sclerosis, mainly through their production of interferon-γ and its effects on macrophage activation and chemokine production. However, this initial concept of T-cell-mediated chronic inflammation required an adjustment with the discovery of an IL-12-related cytokine, designated IL-23. IL-23 was rapidly recognized for its involvement in the establishment of chronic inflammation and in the development of a Th cell subset producing IL-17, designated Th17, which is distinct from the previously reported Th1 and Th2 populations. This review aims to describe the characterization of IL-23 and its receptor, its biological activities, as well as its involvement in the development of human Th17 cells and autoimmunity.