ReviewArthritis research & therapy2008
T-cell co-stimulatory pathways in autoimmunity.
Review in Arthritis research & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis 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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Identification of a costimulatory molecule-based signature for predicting prognosis risk and immunotherapy response in patients with lung adenocarcinoma.Oncoimmunology · 2020Pooled it
- Alternate actions of CDK4/6 inhibitors beyond cell cycle blockade: unexplored roles in therapy resistance.Cancer metastasis reviews · 2025Review
- Comprehensive and advanced T cell cluster analysis for discriminating seropositive and seronegative rheumatoid arthritis.Frontiers in immunology · 2025Article
- Exploring radiation resistance-related genes in pancreatic cancer and their impact on patient prognosis and treatment.Frontiers in immunology · 2025Article
- Advancements in adoptive CAR immune cell immunotherapy synergistically combined with multimodal approaches for tumor treatment.Bioactive materials · 2024Review
- Strengths and limitations of web servers for the modeling of TCRpMHC complexes.Computational and structural biotechnology journal · 2024Article
- Emerging strategies for treating autoimmune disease with genetically modified dendritic cells.Cell communication and signaling : CCS · 2024Review
- Immunogenetics of Systemic Sclerosis.Genes · 2024Review
- Recent Findings on Therapeutic Cancer Vaccines: An Updated Review.Biomolecules · 2024Review
- Regulatory T cells in lung disease and transplantation.Bioscience reports · 2023Review
- Article
- Landscape of costimulatory molecule signature in breast cancer and its prognostic significance.Annals of translational medicine · 2023Article
- The susceptibility of single nucleotide polymorphisms located within co-stimulatory pathways to systemic lupus erythematosus.Frontiers in immunology · 2023Article
- Thymoquinone Effect on Monocyte-Derived Macrophages, Cell-Surface Molecule Expression, and Phagocytosis.Nutrients · 2022Article
- Development and characterization of a novel human CD137 agonistic antibody with anti-tumor activity and a good safety profile in non-human primates.FEBS open bio · 2022Article
- Systems biology models to identify the influence of SARS-CoV-2 infections to the progression of human autoimmune diseases.Informatics in medicine unlocked · 2022Article
- An Integrative Pharmacology Model for Decoding the Underlying Therapeutic Mechanisms of Ermiao Powder for Rheumatoid Arthritis.Frontiers in pharmacology · 2022Article
- CD4Frontiers in immunology · 2022Review
- The association of cervicovaginal Langerhans cells with clearance of human papillomavirus.Frontiers in immunology · 2022Review
- Clinical translation of immunomodulatory therapeutics.Advanced drug delivery reviews · 2021Review
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 1 institution in 1 country.
Funding
Abstract
T-cell activation and differentiation depend on the signal strength received by the T-cell receptor and on signals provided by co-stimulatory molecules. The most prominent co-stimulatory molecule is CD28, which controls the activation of naïve and memory T cells by antigen presented on professional antigen-presenting cells. Blocking of the CD28-CD80/86 pathway has been an appealing strategy for inducing tolerance in autoimmune diseases where the disease-inducing autoantigens are not known. Although CD28 has maintained its unique position, the past decade has witnessed the recognition that a large number of regulatory molecules on T cells must be stimulated to generate a fully protective immune response. These regulatory receptors differ in their preferential expression on T-cell subsets, in the ligands that they recognize, and in the signaling pathways that they trigger. They have in common the fact that they provide information on the cellular environment in which the T-cell response occurs. By intercepting these signals, we may be able to influence disease-relevant T-cell responses in autoimmune diseases while potentially minimizing broad immunosuppression.
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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.