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Interleukin (IL)-17-producing T helper (Th)-17 cells have recently been explained as a distinct population  of  CD4+  T  cells which play an important  role in immunity against infectious agents. Establishment of persistent phenotype of Th17 cells and recognition of lineage-deviating factors are of most attractive goals in modern researches in immunology. Although  IL-6  and  TGF-β  are  frequently used  to  differentiate  naive T  cells to  Th17 phenotype in mouse models, the application of IL-23 and its importance in preventing cells from plasticity needs to be more investigated. Our main objective was to evaluate the role of IL-23 in Th17 to Th1 plasticity. In  this  research  project,  we generated in  vitro  Myelin oligodendrocyte glycoprotein (MOG)-specific Th17 cells in the presence of TGF-β, IL-6, IL-23 and peptide MOG35-55. Th17  development  was confirmed  by assessment  of  relevant  transcription  factors  and secreted cytokines by flowcytometry and ELISA, respectively. Th17 to Th1 plasticity was monitored by consecutive samplings in different time points without any extra supplementation of IL-23. Cell culture supernatant  was evaluated for Interferon  (IFN)-γ secretion and cells were evaluated for intracellular expression of this cytokine. Our results showed that the employed method was relatively convenient in developing antigen-specific Th17  cells. We also showed  that  IL-23  deprivation  which happens  by prolongation of culture period, can convert IL-17 producing cells to IFN-γ secreting Th1 phenotype. IL-23 can be considered as a Th17 phenotype stabilizing factor for in-vitro developed lineages.