ArticleGenes and immunity2016
CD58 mutations are common in Hodgkin lymphoma cell lines and loss of CD58 expression in tumor cells occurs in Hodgkin lymphoma patients who relapse.
Article in Genes and immunity, 2016. 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
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, 55 citations in OpenAlex.
- DUSP6 ablation restores CAR T-cell fitness impaired by tumor CD58 loss through invigoration of AP-1 signaling.Signal transduction and targeted therapy · 2026Article
- CD2 costimulation strength: A key regulator of T cell function and anti-tumor immunity that is epigenetically regulated.iScience · 2025Article
- Platforms for studying cell-cell recognition by immune cells.Immunology and cell biology · 2025Review
- Cancer ATF4-mediated CD58 endocytosis impairs anti-tumor immunity and immunotherapy.Journal of translational medicine · 2025Article
- Mechanistic insights into resistance mechanisms to T cell engagers.Frontiers in immunology · 2025Review
- Revisiting T-cell adhesion molecules as potential targets for cancer immunotherapy: CD226 and CD2.Experimental & molecular medicine · 2024Review
- Genetic ablation of adhesion ligands mitigates rejection of allogeneic cellular immunotherapies.Cell stem cell · 2024Article
- Engineering immune-evasive allogeneic cellular immunotherapies.Nature reviews. Immunology · 2024Review
- Using CombiCells, a platform for titration and combinatorial display of cell surface ligands, to study T-cell antigen sensitivity modulation by accessory receptors.The EMBO journal · 2024Article
- NK Receptors Replace CD28 As the Dominant Source of Signal 2 for Cognate Recognition of Cancer Cells by TAA-specific Effector CD8Research square · 2023Article
- CMTM6 shapes antitumor T cell response through modulating protein expression of CD58 and PD-L1.Cancer cell · 2023Article
- The CD58-CD2 axis is co-regulated with PD-L1 via CMTM6 and shapes anti-tumor immunity.Cancer cell · 2023Article
- Antigen discrimination by T cells relies on size-constrained microvillar contact.Nature communications · 2023Article
- Inefficient exploitation of accessory receptors reduces the sensitivity of chimeric antigen receptors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- PAX5 epigenetically orchestrates CD58 transcription and modulates blinatumomab response in acute lymphoblastic leukemia.Science advances · 2022Article
- Multidimensional single-cell analysis identifies a role for CD2-CD58 interactions in clinical antitumor T cell responses.The Journal of clinical investigation · 2022Article
- Review
- Cancer cell-intrinsic resistance to BiTE therapy is mediated by loss of CD58 costimulation and modulation of the extrinsic apoptotic pathway.Journal for immunotherapy of cancer · 2022Article
- The Emerging Role of CAR T Cell Therapy in Relapsed/Refractory Hodgkin Lymphoma.Journal of personalized medicine · 2022Review
- Characterization of mechanisms positioning costimulatory complexes in immune synapses.iScience · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD58 is involved in immune recognition of tumor cells via binding of the CD2 receptor expressed on cytotoxic T cells. In diffuse large B-cell lymphoma, mutations of the CD58 gene are reported to contribute to immune evasion of the tumor cells. We previously showed CD58 mutations in three Hodgkin lymphoma (HL) cell lines by whole-exome sequencing. In this study, we confirmed the mutations by Sanger sequencing at the DNA and RNA level and showed low levels or total loss of CD58 mRNA expression in two of the three cell lines. CD58 protein expression as determined by flow cytometry, western blotting and immunohistochemistry was absent in all three mutated HL cell lines. In primary tissue samples, loss of CD58 expression was observed in 11% of the patients who relapse. These data suggest that loss of CD58 is a potential immune escape mechanism of HL tumor cells, especially in clinically aggressive disease.
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.