ArticleThe Journal of clinical investigation1998
Host defense molecule polymorphisms influence the risk for immune-mediated complications in chronic granulomatous disease.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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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.
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Who cites it
68 citing papers in PubMed, 241 citations in OpenAlex.
- Article
- ACK1 and BRK non-receptor tyrosine kinase deficiencies are associated with familial systemic lupus and involved in efferocytosis.medRxiv : the preprint server for health sciences · 2024Article
- What can inherited immunodeficiencies reveal about pyoderma gangrenosum?Experimental dermatology · 2024Review
- NCF1-dependent production of ROS protects against lupus by regulating plasmacytoid dendritic cell development and functions.JCI insight · 2023Article
- Fc Receptor Variants and Disease: A Crucial Factor to Consider in the Antibody Therapeutics in Clinic.International journal of molecular sciences · 2021Review
- North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Position Paper on the Evaluation and Management for Patients With Very Early-onset Inflammatory Bowel Disease.Journal of pediatric gastroenterology and nutrition · 2020Article
- Review
- Role of Allogeneic Hematopoietic Stem Cell Transplant for Chronic Granulomatous Disease (CGD): a Report of the United States Immunodeficiency Network.Journal of clinical immunology · 2019Article
- Noninfectious Manifestations and Complications of Chronic Granulomatous Disease.Journal of the Pediatric Infectious Diseases Society · 2018Review
- Altered Humoral Immune Responses and IgG Subtypes in NOX2-Deficient Mice and Patients: A Key Role for NOX2 in Antigen-Presenting Cells.Frontiers in immunology · 2018Article
- The role of monogenic disease in children with very early onset inflammatory bowel disease.Current opinion in pediatrics · 2017Review
- Article
- Nutritional Therapy in Very Early-Onset Inflammatory Bowel Disease: A Case Report.Digestive diseases and sciences · 2017Article
- NADPH Oxidase Deficiency: A Multisystem Approach.Oxidative medicine and cellular longevity · 2017Review
- Article
- Primary immune deficiencies with defects in neutrophil function.Hematology. American Society of Hematology. Education Program · 2016Review
- Genetic Risk for Inflammatory Bowel Disease Is a Determinant of Crohn's Disease Development in Chronic Granulomatous Disease.Inflammatory bowel diseases · 2016Article
- Managing Inflammatory Manifestations in Patients with Chronic Granulomatous Disease.Paediatric drugs · 2016Article
- Subclinical intestinal inflammation in chronic granulomatous disease patients.Immunologic research · 2016Article
- Mannose-binding lectin protein and its association to clinical outcomes in COPD: a longitudinal study.Respiratory research · 2015Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic granulomatous disease (CGD) is an inherited disorder of phagocyte function in which defective superoxide production results in deficient microbicidal activity. CGD patients suffer from recurrent, life-threatening infections, and nearly half develop chronic gastrointestinal (GI) complications (colitis, gastric outlet obstruction, or perirectal abscess) and/or autoimmune/rheumatologic disorders (AIDs). To identify genetic modifiers of disease severity, we studied a cohort of 129 CGD patients, in whom seven candidate genes (myeloperoxidase [MPO], mannose binding lectin [MBL], Fcgamma receptors IIa, IIIa, IIIb, TNF-alpha, and IL-1 receptor antagonist), each containing a physiologically relevant polymorphism predicted to influence the host inflammatory response, were selected for analysis. Genotypes of MPO (P = 0.003) and FcgammaRIIIb (P = 0.007) were strongly associated with an increased risk for GI complications, while an FcgammaRIIa (P = 0.05) genotype was suggestive for an association. Patients with all three associated genotypes had the highest risk for GI complications (P < 0.0001). The risk of AIDs was strongly associated with variant alleles of MBL (P = 0.01) and weakly associated with an FcgammaRIIa genotype (P = 0.04). Patients with variant forms of both MBL and FcgammaRIIa had the highest risk of developing an AID (P = 0.003).
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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.