ArticleProceedings of the National Academy of Sciences of the United States of America2007
Allelic variant in CTLA4 alters T cell phosphorylation patterns.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- CTLA-4 as a genetic determinant in autoimmune Addison's disease.Genes and immunity · 2015Pooled it
- Review
- Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis.The Journal of clinical investigation · 2022Article
- The Immunogenetics of Alopecia areata.Advances in experimental medicine and biology · 2022Article
- Multiple inducers and novel roles of autoantibodies against the obligatory NMDAR subunit NR1: a translational study from chronic life stress to brain injury.Molecular psychiatry · 2021Article
- Some Common SNPs of the T-Cell Homeostasis-Related Genes Are Associated with Multiple Sclerosis, but Not with the Clinical Manifestations of the Disease, in the Polish Population.Journal of immunology research · 2020Article
- T cell costimulation, checkpoint inhibitors and anti-tumor therapy.Journal of biosciences · 2020Review
- On the activation and deactivation pathways of the Lck kinase domain: a computational study.Journal of computer-aided molecular design · 2019Article
- Tipping the balance: inhibitory checkpoints in intestinal homeostasis.Mucosal immunology · 2019Review
- flowVS: channel-specific variance stabilization in flow cytometry.BMC bioinformatics · 2016Article
- CD28 Costimulation: From Mechanism to Therapy.Immunity · 2016Review
- Genetic variants associated with autoimmunity drive NFκB signaling and responses to inflammatory stimuli.Science translational medicine · 2015Article
- Genetic basis of autoimmunity.The Journal of clinical investigation · 2015Review
- Decreased RORC-dependent silencing of prostaglandin receptor EP2 induces autoimmune Th17 cells.The Journal of clinical investigation · 2014Article
- Joint modeling and registration of cell populations in cohorts of high-dimensional flow cytometric data.PloS one · 2014Article
- Role of non-HLA gene polymorphisms in graft-versus-host disease.International journal of hematology · 2013Review
- Matching phosphorylation response patterns of antigen-receptor-stimulated T cells via flow cytometry.BMC bioinformatics · 2012Article
- A computational framework to emulate the human perspective in flow cytometric data analysis.PloS one · 2012Article
- Modulation of cell signaling networks after CTLA4 blockade in patients with metastatic melanoma.PloS one · 2010Article
- Confirmation of the genetic association of CTLA4 and PTPN22 with ANCA-associated vasculitis.BMC medical genetics · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Little is known regarding the functional effects of common autoimmune susceptibility variants on human immune cells. The SNP CT60 (rs3087243; A/G) located in the 3' UTR of the CTLA4 gene has been associated with autoimmune diseases. We examined a cohort of healthy individuals stratified by genotypes at CTLA4 to gain insight into the functional effects of allelic variation on T cell signaling. Using phospho-site-specific mAbs, we tested the hypothesis that the CT60 genotype at CTLA4 is associated with altered T cell antigen receptor (TCR) signaling in naive and/or memory T cells. By normalizing for the extent of the initial TCR signaling event at CD3zeta, we observed that the relative responsiveness to TCR stimulation as assessed by phosphorylation levels of downstream signaling molecules was altered in naive (CD4(+)CD45RA(high)) and memory (CD4(+)CD45RA(low)) T cells obtained from individuals with the disease-susceptibility allele at CTLA4. Thus, allelic variation associated with autoimmune disease can alter the signaling threshold of CD4(+) T cells. These experiments provide a rational approach for the dissection of T cell-susceptibility genes in autoimmune diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.