ArticleJournal of hematology & oncology2016
Molecular alterations in the TCR signaling pathway in patients with aplastic anemia.
Article in Journal of hematology & oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed.
- The Role of Single-Nucleotide Polymorphisms in Acquired Aplastic Anaemia.Scandinavian journal of immunology · 2026Review
- Somatic mutations in CSK disrupt immune regulation in a Chinese aplastic anemia cohort.Communications biology · 2026Article
- Potential of ginsenoside Rg1 to treat aplastic anemiaWorld journal of stem cells · 2024Article
- Sex-Biased CD3ζ 3'-UTR SNP Increased Incidence Risk in Aplastic Anemia.International journal of general medicine · 2024Article
- Anti-Thymocyte Globulin (ATG)-Free Nonmyeloablative Haploidentical PBSCT Plus Post-Transplantation Cyclophosphamide Is a Safe and Efficient Treatment Approach for Pediatric Acquired Aplastic Anemia.International journal of molecular sciences · 2022Article
- Aplastic Anemia as a Roadmap for Bone Marrow Failure: An Overview and a Clinical Workflow.International journal of molecular sciences · 2022Review
- Article
- Abnormal miR-214/A20 expression might play a role in T cell activation in patients with aplastic anemia.Blood science (Baltimore, Md.) · 2020Article
- Genome-wide Association Study Identifies HLA-DPB1 as a Significant Risk Factor for Severe Aplastic Anemia.American journal of human genetics · 2020Article
- MiR-214 regulates CD3ζ expression in T cells.Central-European journal of immunology · 2019Article
- Regulatory γδ T cells induced by G-CSF participate in acute graft-versus-host disease regulation in G-CSF-mobilized allogeneic peripheral blood stem cell transplantation.Journal of translational medicine · 2018Article
- Yin and Yang of mesenchymal stem cells and aplastic anemia.World journal of stem cells · 2017Review
- Deletion with 25 nucleotides ofStem cell investigation · 2017Article
- Aplastic anemia is related to alterations in T cell receptor signaling.Stem cell investigation · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA previous study has demonstrated a significantly increased CD3ζ gene expression level in aplastic anemia (AA). However, the mechanism underlying the upregulated CD3ζ mRNA expression level and that of T cell activation signaling molecules in AA patients remains unclear. Thus, we investigated the expression levels of the CD3ζ, CD28, CTLA-4, and Cbl-b genes, the SNP rs231775 in the CTLA-4 gene, and the distribution of the CD3ζ 3'-UTR splice variant in AA patients.
methodsCD3ζ 3'-UTR splice variants were identified in peripheral blood mononuclear cells (PBMCs) from 48 healthy individuals and 67 patients with AA [37 cases of severe aplastic anemia (SAA) and 30 cases of non-sever aplastic anemia (NSAA)] by RT-PCR. CD3ζ, CD28, CTLA-4, and Cbl-b gene expression was analyzed by real-time quantitative PCR. The SNP rs231775 in CTLA-4 gene was analyzed by PCR-RFLP.
resultsCD3ζ and CD28 expression was significantly higher, while CTLA-4 and Cbl-b expression was significantly lower in AA patients compared with healthy individuals. Significantly higher CD3ζ expression was found in the NSAA subgroup compared with the SAA subgroup. 64 % of the AA samples had the same genotype (WT(+)AS(+)CD3ζ 3'-UTR); 22 % of the AA patients had a WT(+)AS(-)CD3ζ 3'-UTR genotype, and 14 % of the AA patients had a WT(-)AS(+)CD3ζ 3'-UTR genotype. The CD3ζ expression level of WT(-)AS(+) subgroup was the highest in the SAA patients. A significantly higher frequency of the GG genotype (mutant type, homozygous) of SNP rs231775 in CTLA-4 gene was found in the AA patients. Positive correlation between the CTLA-4 and Cbl-b gene expression levels was found in healthy individuals with the AA and AG genotypes, but not in the AA patients.
conclusionsThis is the first study analyzing the expression characteristics of the CD28, CTLA-4, and Cbl-b genes in AA. Our results suggest that aberrant T cell activation may be related to the first and second signals of T cell activation in AA. The GG genotype of SNP rs231775 in CTLA-4 gene might be associated with AA risk in the Chinese population. The characteristics of CD3ζ 3'-UTR alternative splicing may be an index for evaluating the T cell activation status in AA patients, particularly in SAA patients.
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.