ArticlePLoS pathogens2014
P47phox-/- mice are compromised in expansion and activation of CD8+ T cells and susceptible to Trypanosoma cruzi infection.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Glycocalyx-Driven Immunomodulation in Trypanosoma cruzi: Structures, Host Responses, Diagnostic and Therapeutic Targeting.Parasite immunology · 2026Review
- Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Animal models for exploring Chagas disease pathogenesis and supporting drug discovery.Clinical microbiology reviews · 2024Review
- Quantitative Proteomic Analysis of Macrophages Infected withInternational journal of molecular sciences · 2024Article
- Macrophage Polarization and Reprogramming in Acute Inflammation: A Redox Perspective.Antioxidants (Basel, Switzerland) · 2022Review
- Platelets, Macrophages, and Thromboinflammation in Chagas Disease.Journal of inflammation research · 2022Review
- Gasdermins in Innate Host Defense AgainstFrontiers in immunology · 2022Review
- Oxidative stress implications for therapeutic vaccine development against Chagas disease.Expert review of vaccines · 2021Review
- The Redox-Metabolic Couple of T Lymphocytes: Potential Consequences for Hypertension.Antioxidants & redox signaling · 2021Review
- Myeloid-Derived Suppressor Cells inFrontiers in cellular and infection microbiology · 2021Review
- Beyond the Extra Respiration of Phagocytosis: NADPH Oxidase 2 in Adaptive Immunity and Inflammation.Frontiers in immunology · 2021Review
- S100A8 expression in oviduct mucosal epithelial cells is regulated by estrogen and affects mucosal immune homeostasis.PloS one · 2021Article
- The Oxidative Stress and Chronic Inflammatory Process in Chagas Disease: Role of Exosomes and Contributing Genetic Factors.Oxidative medicine and cellular longevity · 2021Review
- Priming Astrocytes With HIV-Induced Reactive Oxygen Species Enhances TheirFrontiers in microbiology · 2020Article
- Article
- Hyperbilirubinemia in Gunn Rats is Associated with Decreased Inflammatory Response in LPS-Mediated Systemic Inflammation.International journal of molecular sciences · 2019Article
- Pathology and Pathogenesis of Chagas Heart Disease.Annual review of pathology · 2019Review
- ROS and Trypanosoma cruzi: Fuel to infection, poison to the heart.PLoS pathogens · 2018Review
- Pathogenesis of Chronic Chagas Disease: Macrophages, Mitochondria, and Oxidative Stress.Current clinical microbiology reports · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Macrophage activation of NAD(P)H oxidase (NOX2) and reactive oxygen species (ROS) is suggested to kill Trypanosoma cruzi that causes Chagas disease. However, the role of NOX2 in generation of protective immunity and whether these mechanisms are deregulated in the event of NOX2 deficiency are not known, and examined in this study. Our data showed that C57BL/6 p47(phox-/-) mice (lack NOX2 activity), as compared to wild-type (WT) mice, succumbed within 30 days post-infection (pi) to low doses of T. cruzi and exhibited inability to control tissue parasites. P47(phox-/-) bone-marrow and splenic monocytes were not compromised in maturation, phagocytosis and parasite uptake capacity. The deficiency of NOX2 mediated ROS was compensated by higher level of inducible nitric oxide synthase (iNOS) expression, and nitric oxide and inflammatory cytokine (TNF-α, IFN-γ, IL-1β) release by p47(phox-/-) macrophages as compared to that noted in WT controls infected by T. cruzi. Splenic activation of Th1 CD4(+)T cells and tissue infiltration of immune cells in T. cruzi infected p47(phox-/-) mice were comparable to that noted in infected control mice. However, generation and activation of type 1 CD8(+)T cells was severely compromised in p47(phox-/-) mice. In comparison, WT mice exhibited a robust T. cruzi-specific CD8(+)T cell response with type 1 (IFN-γ(+)TNF-α>IL-4+IL-10), cytolytic effector (CD8(+)CD107a(+)IFN-γ(+)) phenotype. We conclude that NOX2/ROS activity in macrophages signals the development of antigen-specific CD8(+)T cell response. In the event of NOX2 deficiency, a compromised CD8(+)T cell response is generated, leading to increased parasite burden, tissue pathogenesis and mortality in chagasic mice.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.