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The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.

NOX2 Complex–Derived ROS as Immune Regulators

Open access
Sareila, Outi, Kelkka, Tiina, Pizzolla, Angela, Hultqvist, Malin, Holmdahl, Rikard·2011·Antioxidants & Redox Signaling

Abstract

Reactive oxygen species (ROS) are a heterogeneous group of highly reactive molecules that oxidize targets in a biologic system. During steady-state conditions, ROS are constantly produced in the electron-transport chain during cellular respiration and by various constitutively active oxidases. ROS production can also be induced by activation of the phagocyte NADPH oxidase 2 (NOX2) complex in a process generally referred to as an oxidative burst. The induced ROS have long been considered proinflammatory, causing cell and tissue destruction. Recent findings have challenged this inflammatory role of ROS, and today, ROS are also known to regulate immune responses and cell proliferation and to determine T-cell autoreactivity. NOX2-derived ROS have been shown to suppress antigen-dependent T-cell reactivity and remarkably to reduce the severity of experimental arthritis in both rats and mice. In this review, we discuss the role of ROS and the NOX2 complex as suppressors of autoimmunity, inflammation, and arthritis.

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Metadata

Authors
Sareila, O., Kelkka, T., Pizzolla, A., Hultqvist, M., & Holmdahl, R.
Venue
Antioxidants & Redox Signaling
Published
2011-10-15
Volume
15
Issue
8
Pages
2197-2208
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
OpenAlex
W2067555058
Cited by
200
References
13
FWCI
5.62
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: NOX2 Complex–Derived ROS as Immune Regulators. https://app.cochat.ai/papers/10.1089/ars.2010.3635
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Sareila, O., Kelkka, T., Pizzolla, A., Hultqvist, M., & Holmdahl, R. (2011). NOX2 Complex–Derived ROS as Immune Regulators. Antioxidants & Redox Signaling. https://doi.org/10.1089/ars.2010.3635

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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