ArticleEuropean journal of immunology2011
Adaptive immune defects against glycoantigens in chronic granulomatous disease via dysregulated nitric oxide production.
Article in European journal of immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Atopy and immune dysregulation among patients with chronic granulomatous disease.Frontiers in immunology · 2025Article
- The Multiple Faces of Nitric Oxide in Chronic Granulomatous Disease: A Comprehensive Update.Biomedicines · 2022Review
- Dendritic cell-specific Mgat2 knockout mice show antigen presentation defects but reveal an unexpected CD11c expression pattern.Glycobiology · 2016Article
- Polysaccharide A from the capsule of Bacteroides fragilis induces clonal CD4+ T cell expansion.The Journal of biological chemistry · 2015Article
- Heat Shock Protein 60 in Eggs Specifically Induces Tregs and Reduces Liver Immunopathology in Mice with Schistosomiasis Japonica.PloS one · 2015Article
- Deficient production of reactive oxygen species leads to severe chronic DSS-induced colitis in Ncf1/p47phox-mutant mice.PloS one · 2014Article
- Neutrophils confer T cell resistance to myeloid-derived suppressor cell-mediated suppression to promote chronic inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic granulomatous disease (CGD) is a primary immunodeficiency defined by mutations in the NADPH oxidase complex leading to reduced superoxide production, increased susceptibility to infection, chronic inflammation, and recurring abscess and granuloma formation. Here, we found that CGD mice were hyperresponsive to abscess-inducing T-cell-dependent carbohydrate antigens (glycoantigens) due to a ten-fold increase in NO production within APCs, which is known to be necessary for glycoantigen presentation on MHC class II. CGD mice exhibited increased Th1 pro-inflammatory T-cell responses in vitro and in vivo, characterized by more severe abscess pathology. This phenotype was also seen in WT animals following adoptive transfer of neutrophil-depleted APCs from CGD animals, demonstrating that this phenotype was independent of neutrophil and T-cell defects. Finally, pharmacological attenuation of NO production to WT levels in vivo reduced abscess incidence and severity in CGD without overt increases in inflammation or the ability to clear infection, suggesting a potential new treatment option for early stage CGD-associated infections.
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Registered trials
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.