ArticleCellular and molecular life sciences : CMLS2015
In the absence of its cytosolic domain, the CD28 molecule still contributes to T cell activation.
Article in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Advances in CAR optimization strategies based on CD28.Frontiers in immunology · 2025Review
- Lymphotoxin limits Foxp3Nature communications · 2024Article
- CD28 costimulation promotes an antitumor CD8Cellular & molecular immunology · 2022Article
- Identification of Potent CD19 scFv for CAR T Cells through scFv Screening with NK/T-Cell Line.International journal of molecular sciences · 2020Article
- Chimeric antigen receptor T-cell therapy in glioblastoma: charging the T cells to fight.Journal of translational medicine · 2020Review
- The promise of chimeric antigen receptor (CAR) T cell therapy in multiple myeloma.Cellular immunology · 2019Review
- Review
- Engineering and Design of Chimeric Antigen Receptors.Molecular therapy. Methods & clinical development · 2019Review
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 at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CD28 costimulatory receptor has a pivotal role in T cell biology as this molecule amplifies T cell receptor (TCR) signals to provide an efficient immune T cell response. There is a large debate about how CD28 mediates these signals. Here, we designed a CD28 gene-targeted knock-in mouse strain lacking the cytoplasmic tail of CD28. As is the case in CD28-deficient (CD28 knock-out) mice, regulatory T cell homeostasis and T cell activation are altered in these CD28 knock-in mice. Unexpectedly, the presence of a CD28 molecule deprived of its cytoplasmic tail could partially induce some early activation events in T cells such as signaling events or expression of early activation markers. These results unravel a new mechanism of T cell costimulation by CD28, independent of its cytoplasmic tail.
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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.