Abstract
Abstract Nox2/gp91phox, one of phagocyte NADPH oxidase subunits, is mainly expressed on phagocytes. They transport electrons across the plasma membranes and kill pathogens by producing ROS. Many evidences have shown that Nox2 deficiency causes susceptibility to infections and immunosuppression. Recent studies have identified functional phagocyte-type Nox2 is also expressed in helper T cells through TCR stimulation. So, many papers attempted to define the role of Nox2 on Th1 and Th17 cell differentiation, but the exact function of Nox2 in Th2 differentiation remains unclear. To elucidate this, we adopted experimental allergic asthma that Th2 cells have been considered as a pivotal mediator for asthma pathogenesis. Here, we revealed that Nox2 deficient mice showed enhanced allergic asthma phenotypes including increased airway hyper responsiveness, eosinophilia, glycoprotein secretion and IL-4 production in bronchoalveolar lavage through augmented Th2 differentiation, regardless of challenge routes and allergen types. Based on our results, we conclude that Nox2 could be a molecular target for controlling Th2 cell differentiation and allergic asthma.
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