Fig. 8: Model for Fas/FasL regulating mROS and IFN-γ production after IL-12/IL-18 stimulation. | Cell Death & Disease

Fig. 8: Model for Fas/FasL regulating mROS and IFN-γ production after IL-12/IL-18 stimulation.

From: Mitochondrial reactive oxygen is critical for IL-12/IL-18-induced IFN-γ production by CD4+ T cells and is regulated by Fas/FasL signaling

Fig. 8

Left, IL-12/IL-18 stimulation triggers mitochondria activation and mROS production, which activate the pathway leading to IFN-γ expression. Fas/FasL interaction leads to cytochrome C release, which controls mitochondrial activity and mROS production [39] and, consequently, IFN-γ. Caspase-3 is located outside of mitochondria [58], but there is no apoptosis induction in response to IL-12/IL-18. Right, In absence of Fas, cytochrome C is retained in mitochondria and mROS production is increased. Fas deficiency provokes caspase-3 translocation to mitochondria after IL-12/IL-18 stimulation, which might further increase mROS production [54]. Overall, increased mROS production results in IFN-γ hyperproduction in absence of Fas/FasL interaction.

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