ReviewSpringer seminars in immunopathology1998
The molecular basis of chronic granulomatous disease.
Review in Springer seminars in immunopathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 114 citations in OpenAlex.
- Five CGD-Linked CYBB Mutations in Chinese Patients: Insights Into Predicting IFN-γ Treatment Efficacy.Journal of clinical immunology · 2025Article
- STAT4 is expressed in neutrophils and promotes antimicrobial immunity.JCI insight · 2021Article
- Redox regulation of immunometabolism.Nature reviews. Immunology · 2021Review
- An adult autosomal recessive chronic granulomatous disease patient with pulmonary Aspergillus terreus infection.BMC infectious diseases · 2018Article
- Differential diagnosis in ulcerative colitis in an adolescent: Chronic granulomatous disease needs extra attention.World journal of gastrointestinal pathophysiology · 2017Article
- Roles for retrotransposon insertions in human disease.Mobile DNA · 2016Review
- Increased NADPH oxidase-derived superoxide is involved in the neuronal cell death induced by hypoxia-ischemia in neonatal hippocampal slice cultures.Free radical biology & medicine · 2012Article
- NF-kappaB protects cells from gamma interferon-induced RIP1-dependent necroptosis.Molecular and cellular biology · 2011Article
- p47phox, the phagocyte NADPH oxidase/NOX2 organizer: structure, phosphorylation and implication in diseases.Experimental & molecular medicine · 2009Review
- Chronic granulomatous disease: the European experience.PloS one · 2009Article
- Hyperinflammation in chronic granulomatous disease and anti-inflammatory role of the phagocyte NADPH oxidase.Seminars in immunopathology · 2008Review
- Phosphatidylinositol 3-phosphate-dependent and -independent functions of p40phox in activation of the neutrophil NADPH oxidase.The Journal of biological chemistry · 2008Article
- Successful unrelated bone marrow transplantation in a child with chronic granulomatous disease complicated by pulmonary and cerebral granuloma formation.European journal of pediatrics · 2007Article
- PtdIns3P binding to the PX domain of p40phox is a physiological signal in NADPH oxidase activation.The EMBO journal · 2006Article
- Chronic Granulomatous Disease; fundamental stages in our understanding of CGD.Medical immunology (London, England) · 2006Article
- Neutrophils from p40phox-/- mice exhibit severe defects in NADPH oxidase regulation and oxidant-dependent bacterial killing.The Journal of experimental medicine · 2006Article
- Anaplasma phagocytophilum modulates gp91phox gene expression through altered interferon regulatory factor 1 and PU.1 levels and binding of CCAAT displacement protein.Infection and immunity · 2005Article
- Genomic characterization of recent human LINE-1 insertions: evidence supporting random insertion.Genome research · 2001Article
- Contribution of Mn-cofactored superoxide dismutase (SodA) to the virulence of Streptococcus agalactiae.Infection and immunity · 2001Article
- Ascaris suum-derived products induce human neutrophil activation via a G protein-coupled receptor that interacts with the interleukin-8 receptor pathway.Infection and immunity · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CGD is a rare inherited immunodeficiency syndrome, caused by the phagocytes' inability to produce (sufficient) reactive oxygen metabolites. This dysfunction is due to a defect in the NADPH oxidase, the enzyme responsible for the production of superoxide. It is composed of several subunits, two of which, gp91phox and p22phox, form the membrane-bound cytochrome b558, while its three cytosolic components, p47phox, p67phox and p40phox, have to translocate to the membrane upon activation. This is a tightly and intricately controlled process that involves, among others, several low-molecular weight GTP-binding proteins. Gp91phox is encoded on the X-chromosome and p22phox, p47phox and p67phox on different autosomal chromosomes, and a defect in one of these components leads to CGD. This explains the variable mode of inheritance seen in this syndrome. Clinically CGD manifests itself typically already at a very young age with recurrent and serious infections, most often caused by catalase-positive pathogens. Modern treatment options, including prophylaxis with trimethoprim-sulfamethoxazole and rIFN-gamma as well as early and aggressive anti-infection therapy, have improved the prognosis of this disease dramatically. CGD, as a very well-characterized inherited affection of the hematopoietic stem cells, is predestined to be among the first diseases to profit from the advances in cutting-edge therapeutics, such as gene therapy and in utero stem cell transplantation.
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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.