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Article

NOX2 deficiency alters macrophage phenotype through an IL-10/STAT3 dependent mechanism: implications for traumatic brain injury.

Journal of neuroinflammation - 24 Mar 2017

Barrett James P, Henry Rebecca J, Villapol Sonia, Stoica Bogdan A, Kumar Alok, Burns Mark P, Faden Alan I, Loane David J

Abstract excerpt

BACKGROUND: NADPH oxidase (NOX2) is an enzyme system that generates reactive oxygen species (ROS) in microglia and macrophages. Excessive ROS production is linked with neuroinflammation and chronic neurodegeneration following traumatic brain injury (TBI). Redox signaling regulates macrophage/microglial phenotypic responses (pro-inflammatory versus anti-inflammatory), and NOX2 inhibition following...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 28340575
DOI: 10.1186/s12974-017-0843-4
PMCID: PMC5366128

Genes

STAT3
STAT6
STAT1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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