Human Genetic GLUT1 Deficiency Results in Impaired T Cellular IFN-γ Production.

GLUT1 deficiency prevents glucose uptake in T cells resulting in lower intracellular ATP generation and IFNy production.

NRF2/Itaconate Axis Regulates Metabolism and Inflammatory Properties of T Cells in Children with JIA.

Background: CD4+ T cells critically contribute to the initiation and perturbation of inflammation. When CD4+ T cells enter inflamed tissues, they adapt to hypoxia and oxidative stress conditions, and to a reduction in nutrients. We aimed to investigate how this distinct environment regulates T cell responses within the inflamed joints of patients with childhood rheumatism (JIA) by analyzing the behavior of NRF2-the key regulator of the anti-oxidative stress response-and its signaling pathways.

miR-23a contributes to T cellular redox metabolism in juvenile idiopathic oligoarthritis.

Objective: JIA is a chronic inflammatory disease of unknown origin. The regulation of inflammatory processes involves multiple cellular steps including mRNA transcription and translation. Different miRNAs control these processes tightly.

Nrf2 expression driven by Foxp3 specific deletion of Keap1 results in loss of immune tolerance in mice.

The transcription factor Nrf2 regulates oxidative stress responses. However, the specific function of Nrf2 in Tregs, the central regulators of immune homeostasis, is unclear. Here, we report an unexpected but important role of Nrf2 in Tregs.