Skip to main content
Fig. 4 | Inflammation and Regeneration

Fig. 4

From: Induced pluripotent stem cells representing Nakajo-Nishimura syndrome

Fig. 4

Scheme of the autoinflammatory pathomechanism in NNS. In NNS-type-mutated PSC-MLs, the ROS productions as well as the accumulation of ubiquitinated proteins are constitutively induced by the iP dysfunction. The STAT1 phosphorylation contributed by ROS, accompanied by the p38-MAPK phosphorylation, provides the “priming” inflammatory signal. After IFN-γ plus TNF-α-stimulation, any of a pan-JAK inhibitor, a p38-MAPK inhibitor, and antioxidants significantly reduced both IL-6 and IP-10 secretion, suggesting a pathological crosstalk between the IFN-JAK-STAT-IP-10 pathway and the TNF-α-p38-MAPK-IL-6 pathway

Back to article page