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Kristi Clark (Tisch MS) presented the following article in Journal Club.
Article Title: The Encephalitogenicity of T(H)17 Cells is Dependent on IL-1- and IL-23-Induced Production of the Cytokine GM-CSF
Reference: M. El-Behi, B. Ciric, H. Dai, Y. Yan, M. Cullimore, F. Safavi, G. Zhang, B. Dittel, and A. Rostami. Nature Immunology (2011) vol. 12 no. 6, pp. 568-676.
Interleukin 17 (IL-17)-producing helper T cells (TH17 cells) require exposure to IL-23 to become encephalitogenic, but the mechanism by which IL-23 promotes their pathogenicity is not known. The authors of the present paper found that IL-23 induced production of the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) in TH17 cells and that GM-CSF had an essential role in their encephalitogenicity. Their 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 TH17 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 TH17 cells as a crucial source of GM-CSF in autoimmune inflammation.