Trial reportImmunology2013
CD26-mediated co-stimulation in human CD8(+) T cells provokes effector function via pro-inflammatory cytokine production.
Trial report in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 88 citations in OpenAlex.
- Dipeptidyl Peptidase 4 Inhibition for Prophylaxis of Acute Graft-versus-Host Disease.The New England journal of medicine · 2021Trial
- CD8Nature reviews. Cardiology · 2026Review
- DPP-4 Inhibitors in Female Cancers: Opportunities for Drug Repurposing.Current issues in molecular biology · 2026Review
- Review
- A Novel Polymersome Nanocarrier Promotes Anti-Tumour Immunity by Improved Priming of CD8Immunology · 2025Article
- Optimal GVHD Prophylaxis.Advances in experimental medicine and biology · 2025Review
- Selective refueling of CAR T cells using ADA1 and CD26 boosts antitumor immunity.Cell reports. Medicine · 2024Article
- ADA/CD26 axis increases intra-tumor PD-1Oncoimmunology · 2024Article
- Protein Kinase C at the Crossroad of Mutations, Cancer, Targeted Therapy and Immune Response.Biology · 2023Review
- Impact of standard-dose dipeptidyl peptidase-4 inhibitors on the incidence of graft-versus-host disease after allogeneic hematopoietic cell transplantation.Bone marrow transplantation · 2023Article
- Depletion of polyfunctional CD26Experimental hematology & oncology · 2023Article
- Flow cytometric characterization of cell surface markers to differentiate between fibroblasts and mesenchymal stem cells of different origin.Archives of medical science : AMS · 2023Article
- CD26Frontiers in immunology · 2023Article
- Patients With Severe Multiple Sclerosis Exhibit Functionally Altered CD8Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- Does DPP-IV Inhibition Offer New Avenues for Therapeutic Intervention in Malignant Disease?Cancers · 2022Review
- The Multiple Biological Functions of Dipeptidyl Peptidase-4 in Bone Metabolism.Frontiers in endocrinology · 2022Review
- An update on the interaction between COVID-19, vaccines, and diabetic kidney disease.Frontiers in immunology · 2022Review
- Emerging Role of Dipeptidyl Peptidase-4 in Autoimmune Disease.Frontiers in immunology · 2022 · on this mapReview
- SARS-CoV-2 and diabetes: A potential therapeutic effect of dipeptidyl peptidase 4 inhibitors in diabetic patients diagnosed with COVID-19.Metabolism open · 2021Article
- Review
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD26 is an activation marker of human CD4(+) T cells, and is associated with T-cell signal transduction processes as a co-stimulatory molecule. We have previously demonstrated that high CD26 cell surface expression on CD4(+) T cells is correlated with the production of T helper type 1 cytokines, whereas CD26(+) T helper cells stimulate antibody synthesis in B cells. Although the cellular and molecular mechanisms involved in CD26-mediated CD4(+) T-cell activation have been extensively evaluated by our group and others, the role of CD26 in CD8(+) T cells has not been clearly elucidated. In the present study, we examine the effector function of CD8(+) T cells via CD26-mediated co-stimulation in comparison with CD28-mediated co-stimulation. We found that CD26(high) CD8(+) T cells belong to the early effector memory T-cell subset, and that CD26-mediated co-stimulation of CD8(+) T cells exerts a cytotoxic effect preferentially via granzyme B, tumour necrosis factor-α, interferon-γ and Fas ligand. The effector function associated with CD26-mediated co-stimulation is enhanced compared with that obtained through CD28-mediated co-stimulation, suggesting that the CD26 co-stimulation pathway in CD8(+) T cells is distinct from the CD28 co-stimulation pathway. Targeting CD26 in CD8(+) T cells therefore has the potential to be useful in studies of immune responses to new vaccine candidates as well as innovative therapy for immune-mediated 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.