Influence of a mutation in IFN-γ receptor 2 (IFNGR2) in human cells on the generation of Th17 cells in memory T cells

The T cell subsets involved in inflammatory reactions are mainly the IFN-gamma secreting Th1 cells and IL17-producing Th17 cells. Although Th17 cells are primed in the thymus, there is evidence that Th17 cells can be generated from effector memory CD4(+) T cells. Cytokines as IL-6, TGF-beta, IL-21 and IL-23 involved in development of Th17 cells are well described. Here we analyzed the impact of a mutation in the IFN-gamma receptor 2 (IFN-gamma R2) on the induction of Th17 cells. By isolation of T cells and monocytes of a patient with this mutation we could demonstrate an inhibitory role of IFN-gamma signaling as IFN-gamma R2-deficient monocytes induce a higher percentage of IL-17(+) cells from both healthy and IFN-gamma R2-deficient CD4(+) T cells. This data confirm the interference of these two T helper subsets and points to a balance of Thl and Th17 cells obtained by their own cytokine production and their interplay with APCs. (c) 2013 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.