Interleukin-17 and its target genes: mechanisms of interleukin-17 function in disease
Article first published online: 2 FEB 2010
© 2010 Blackwell Publishing Ltd
Volume 129, Issue 3, pages 311–321, March 2010
How to Cite
Onishi, R. M. and Gaffen, S. L. (2010), Interleukin-17 and its target genes: mechanisms of interleukin-17 function in disease. Immunology, 129: 311–321. doi: 10.1111/j.1365-2567.2009.03240.x
- Issue published online: 2 FEB 2010
- Article first published online: 2 FEB 2010
- Received 19 November 2009; revised 3 December 2009; accepted 15 December 2009.
- gene target;
- signal transduction
Interleukin-17 (IL-17) has emerged as a central player in the mammalian immune system. Although this cytokine exerts a host-defensive role in many infectious diseases, it promotes inflammatory pathology in autoimmunity and other settings. A myriad of studies have focused on how IL-17-producing cells are generated. However, the means by which IL-17 achieves its effects, either for the benefit or the detriment of the host, are due in large part to the induction of new gene expression. Whereas many IL-17 target genes are common to different disease states, in some cases the effects of IL-17 differ depending on the target cell, infectious site or pathogen. Gene products induced by IL-17 include cytokines (IL-6, granulocyte-colony-stimulating factor, tumour necrosis factor-α), chemokines (CXCL1, CXCL2, CCL20, among many others), inflammatory effectors (acute-phase protesins, complement) and antimicrobial proteins (defensins, mucins). Different cell types appear to respond differently to IL-17 in terms of target gene expression, with notable differences seen in mesenchymal and epithelial cells compared with cells of haematopoietic origin. Here, we summarize the major IL-17 target genes that mediate this cytokine’s activities in both autoimmune and chronic diseases as well as during various types of infections.