NADPH oxidase 2 is a superoxide-generating enzymatic complex based on the catalytic subunit gp91phox that is also known as Nox2. Initially identified in neutrophils, NADPH oxidase 2 was long considered responsible only for the killing of phagocytized microorganisms. However, advances in knowledge about redox signalling and the discovery of Nox2 expression in different cell types, including macrophages, endothelial cells (ECs), dendritic cells (DCs), B and T lymphocytes, have changed this paradigm. For instance, Nox2 expressed in macrophages and neutrophils limits the transcription of cytokines and toll-like receptors (TLRs) induced by lipopolysaccharide (LPS), whereas DC Nox2 facilitates antigen cross-presentation to T cells. More recently, our group observed that Nox2 inhibits the suppressive ability of regulatory T cells (Tregs) by limiting NF-κB and FoxP3 activation. In this review, we discuss non-canonical microbicidal functions and redox-signalling-associated roles of Nox2 in different cell types, emphasizing its roles in the innate and adaptive immune system.

中文翻译：

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除了杀灭细菌：NADPH 氧化酶 2 是一种免疫调节剂。

NADPH 氧化酶 2 是一种基于催化亚基 gp91phox（也称为 Nox2）的超氧化物酶复合物。最初在中性粒细胞中发现，NADPH 氧化酶 2 长期以来被认为仅负责杀死被吞噬的微生物。然而，有关氧化还原信号传导的知识的进步以及 Nox2 在不同细胞类型（包括巨噬细胞、内皮细胞 (EC)、树突细胞 (DC)、B 和 T 淋巴细胞）中表达的发现已经改变了这一范式。例如，在巨噬细胞和中性粒细胞中表达的 Nox2 限制了脂多糖 (LPS) 诱导的细胞因子和 Toll 样受体 (TLR) 的转录，而 DC Nox2 促进了抗原向 T 细胞的交叉呈递。最近，我们小组观察到 Nox2 通过限制 NF-κB 和 FoxP3 激活来抑制调节性 T 细胞 (Tregs) 的抑制能力。在这篇综述中，我们讨论了 Nox2 在不同细胞类型中的非典型杀菌功能和氧化还原信号相关作用，强调了它在先天性和适应性免疫系统中的作用。