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Title 

Enhanced Th2 cell differentiation and function in the absence of Nox2

Authors 

B I KwonT W KimK ShinY H KimC M YukJ M YukD M ShinE K JoChul Ho LeeS H Lee

Publisher 

Wiley

Issue Date 

2017

Citation 

Allergy

Keywords 

AKTallergic asthmamitochondrial ROSNox2Th2 cell

Abstract 

Background: Patients with chronic granulomatous disease (CGD), whom inherit abnormal function of NADPH oxidase 2 (Nox2), suffer from hyperinflammatory responses in lung as well as bacterial and fungal infection. There have been studies to reveal the function of Nox2 in hyperinflammatory diseases, especially in asthma, but the exact role of Nox2 in asthma is still unclear and controversial. Therefore, we attempted to clarify the exact role of Nox2 in asthma, using various experimental asthma models. Methods: Asthma phenotypes were analyzed in response to various allergen-induced experimental asthma using Nox2-deficient mice and recombinase gene-activating-1-deficient mice. To understand the underlying mechanisms of exaggerated Th2 effector functions, we investigated the degree of T-cell activation, levels of activation-induced cell death (AICD), and regulatory T (Treg)-cell differentiation in Nox2-deficient T cells. Results: Asthma phenotypes were increased through enhanced Th2 differentiation and function in Nox2-null mice regardless of dose and route of various allergens. Nox2-deficient T cells also showed hyperactivation, reduced AICD, and diminished Treg-cell differentiation through increased AKT phosphorylation (T308/S473) and enhanced mitochondrial ROS production. Conclusion: Our findings indicate that Nox2 deficiency results in exaggerated experimental asthma, which is caused by enhanced Th2 effector function in a T-cell-intrinsic manner.

ISSN 

0105-4538

Link 

http://dx.doi.org/10.1111/all.12944

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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