Abstract
Interleukin 17 (IL-17)-producing helper T cells (TH 17 cells) require exposure to IL-23 to become encephalitogenic, but the mechanism by which IL-23 promotes their pathogenicity is not known. Here we found that IL-23 induced production of the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) in TH 17 cells and that GM-CSF had an essential role in their encephalitogenicity. Our findings identify a chief mechanism that underlies the important role of IL-23 in autoimmune diseases. IL-23 induced a positive feedback loop whereby GM-CSF secreted by TH 17 cells stimulated the production of IL-23 by antigen-presenting cells. Such cross-regulation of IL-23 and GM-CSF explains the similar pattern of resistance to autoimmunity when either of the two cytokines is absent and identifies T H 17 cells as a crucial source of GM-CSF in autoimmune inflammation.
Original language | English (US) |
---|---|
Pages (from-to) | 568-575 |
Number of pages | 8 |
Journal | Nature Immunology |
Volume | 12 |
Issue number | 6 |
DOIs | |
State | Published - Jun 2011 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology