ArticleGenes and immunity2009
Remapping the type I diabetes association of the CTLA4 locus.
Article in Genes and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 52 citations in OpenAlex.
- Emerging new immune checkpoint inhibitors in solid tumor immunotherapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Advancing Understanding of Epilepsy and Type 1 Diabetes Mellitus: A Global Perspective on Research Trends and Future Directions.Journal of diabetes research · 2025Article
- Diminished LAG3Annals of medicine · 2023Article
- Reduced Number of Thymoma CTLA4-Positive Cells Is Associated With a Higher Probability of Developing Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Association of HLA-DQ Heterodimer Residues -18β and β57 With Progression From Islet Autoimmunity to Diabetes in the Diabetes Prevention Trial-Type 1.Diabetes care · 2022Article
- Immune-Checkpoint Expression on CD4, CD8 and NK Cells in Blood, Bronchoalveolar Lavage and Lymph Nodes of Sarcoidosis.Molecular diagnosis & therapy · 2022Article
- Improved genetic risk scoring algorithm for type 1 diabetes prediction.Pediatric diabetes · 2022Article
- Functional Impact of Risk Gene Variants on the Autoimmune Responses in Type 1 Diabetes.Frontiers in immunology · 2022Review
- Serum sCTLA-4 level is not associated with type 1 diabetes or the coexistence of autoantibodies in children and adolescent patients from the southern region of Saudi Arabia.Auto- immunity highlights · 2020Article
- The yin and yang of co-inhibitory receptors: toward anti-tumor immunity without autoimmunity.Cell research · 2020Review
- Gestational respiratory infections interacting with offspring HLA and CTLA-4 modifies incident β-cell autoantibodies.Journal of autoimmunity · 2018Article
- Are Regulatory T Cells Defective in Type 1 Diabetes and Can We Fix Them?Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- T-cell exhaustion: understanding the interface of chronic viral and autoinflammatory diseases.Immunology and cell biology · 2016Review
- CD28 Costimulation: From Mechanism to Therapy.Immunity · 2016Review
- Lag-3, Tim-3, and TIGIT: Co-inhibitory Receptors with Specialized Functions in Immune Regulation.Immunity · 2016Review
- A bispecific protein capable of engaging CTLA-4 and MHCII protects non-obese diabetic mice from autoimmune diabetes.PloS one · 2013Article
- Improving power of genome-wide association studies with weighted false discovery rate control and prioritized subset analysis.PloS one · 2012Article
- Replication and further characterization of a Type 1 diabetes-associated locus at the telomeric end of the major histocompatibility complex.Journal of diabetes · 2011Article
- Association between type 1 diabetes and GWAS SNPs in the southeast US Caucasian population.Genes and immunity · 2011Article
- Proceedings of the Tenth Annual UT-ORNL-KBRIN Bioinformatics Summit 2011.BMC bioinformatics · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The Type I Diabetes Genetics Consortium genotyped 24 single-nucleotide polymorphisms (SNPs) in the CTLA4 locus in 2298 type I diabetes (T1D) nuclear families (11 159 individuals, 5003 affected) to evaluate the recognized T1D association. The 24 CTLA4 SNPs span approximately 43 kb from the 5' flanking to 3' flanking region of the gene in the middle of an extended region of linkage disequilibrium of more than 100 kb. The genotyping was performed using two technologies (Illumina GoldenGate and Sequenom iPlex) on the same samples. The genotype calls by both the methods were highly consistent (the majority >99%). Previously reported T1D association from both the +49G>A and the CT60 SNPs was replicated. The reported association of the -319C>T SNP was not replicated. Although associated with T1D risk, it is likely that neither SNP is causative, as the peak of T1D association was from the SNP rs231727 at 3' flanking of the CTLA4 gene. Comprehensive resequencing and fine mapping of the CTLA4 region are still needed to clarify the causal variants.
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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.