ReviewTrends in immunology2015
Confusing signals: recent progress in CTLA-4 biology.
Review in Trends in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 211 papers, 2 of them syntheses 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
211 citing papers in PubMed, 2 syntheses or guidelines pooled it, 341 citations in OpenAlex.
- Association betweenAging · 2021Pooled it
- CTLA-4 +49 G/A, a functional T1D risk SNP, affects CTLA-4 level in Treg subsets and IA-2A positivity, but not beta-cell function.Scientific reports · 2018Pooled it
- Engineered CTLA-4 targeting chimeras for targeted protein degradation and immune synapse reprogramming.bioRxiv : the preprint server for biology · 2026Article
- Decoding TNF receptor superfamily control of CD4Cell communication and signaling : CCS · 2026Review
- Landscape of T-cell bispecific antibodies in cancer therapy: therapeutic strategies, challenges and future prospection.Molecular cancer · 2026Review
- LRBA organizes distinct vesicular trafficking systems in distal nephron segments for water and sodium conservation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Radiogenomic landscape of the hallmarks of cancer.Biomarker research · 2026Review
- Molecular immune signature identifies microglia and NK cell infiltration as a favorable prognostic marker in adult-type high-grade glioma.ESMO open · 2026Article
- Th17/Treg cell imbalance in allergic rhinitis: mechanisms and therapeutic implications.Genes and immunity · 2026Review
- Unraveling Immune Checkpoint Inhibitor-Associated Cardiovascular Toxicities: Pathway Insights, Mechanisms, and Emerging Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- T Cell Exhaustion in Hepatocellular Carcinoma: A Substantial Barrier in Immunotherapy.Journal of cellular and molecular medicine · 2026Review
- CRISPR/Cas9 Technology for Modifying Immune Checkpoint in CAR-T Cell Therapy for Hematopoietic Malignancies.Current gene therapy · 2026Review
- Treg-microglia crosstalk in Alzheimer's disease: stage-dependent dynamics, molecular mechanisms, and translational challenge.Frontiers in aging neuroscience · 2026Review
- Harnessing tumor immune checkpoints for autoimmune disease therapeutics.Frontiers in immunology · 2026Review
- Thirty years in, regulatory T cells are ready for medicine.Frontiers in immunology · 2026Review
- Proteostasis of immune checkpoint receptors.The Biochemical journal · 2025Review
- Article
- IRnet: Immunotherapy response prediction using pathway knowledge-informed graph neural network.Journal of advanced research · 2025Article
- Pan-cancer analysis of ITGB3 as a potential prognostic and immunological biomarker.Discover oncology · 2025Article
- Molecular biology of the novel anticancer medications: a focus on kinases inhibitors, biologics and CAR T-cell therapy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
151 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanism of action of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) remains surprisingly unclear. Regulatory T (Treg) cells can use CTLA-4 to elicit suppression; however, CTLA-4 also operates in conventional T cells, reputedly by triggering inhibitory signals. Recently, interactions mediated via the CTLA-4 cytoplasmic domain have been shown to preferentially affect Treg cells, yet other evidence suggests that the extracellular domain of CTLA-4 is sufficient to elicit suppression. Here, we discuss these paradoxical findings in the context of CTLA-4-mediated ligand regulation. We propose that the function of CTLA-4 cytoplasmic domain is not to transmit inhibitory signals but to precisely control the turnover, cellular location, and membrane delivery of CTLA-4 to facilitate its central function: regulating the access of CD28 to their shared ligands.
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.