ReviewArthritis research2002
Studies of T-cell activation in chronic inflammation.
Review in Arthritis research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 134 citations in OpenAlex.
- Differential Expression of Cytotoxic-Associated Markers in Circulating CD4International journal of molecular sciences · 2026Article
- The Scent of a Therapy for Spinal Cord Injury: Growth Factors and Their Potential to Modulate Olfactory Ensheathing Cells.Biomolecules · 2026Review
- Revealing the role of natural killer cells in ankylosing spondylitis: identifying diagnostic biomarkers and therapeutic targets.Annals of medicine · 2025Article
- Microneurotrophin BNN27 Exerts Significant Anti-Inflammatory Effects on Murine T-Lymphocytes Following CFA-Induced Inflammatory Pain.International journal of molecular sciences · 2025Article
- The unexplored relationship between spontaneous osteoclastogenesis and platelets in osteoporosis.Frontiers in medicine · 2025Article
- The role of immune checkpoints PD-1 and CTLA-4 in cardiovascular complications leading to heart failure.Frontiers in immunology · 2025Review
- Increased circulating Th17 cells and altered CD4 T cell maturation and differentiation in active tuberculosis with type 2 diabetes: a pilot study.Frontiers in immunology · 2025Article
- Identification of key hub genes in knee osteoarthritis through integrated bioinformatics analysis.Scientific reports · 2024Article
- Integrating MICRORNA941 and T cell subset research into public health strategies for managing inflammaging in elderly and immune-compromised patients.Bioinformation · 2024Article
- Cytokines in Systemic Lupus Erythematosus-Focus on TNF-α and IL-17.International journal of molecular sciences · 2023Review
- Acute inflammation alters lung lymphocytes and potentiates innate-like behavior in young mouse lung CD8 T cells, resembling lung CD8 T cells from old mice.Journal of leukocyte biology · 2023Article
- Cell Trafficking at the Intersection of the Tumor-Immune Compartments.Annual review of biomedical engineering · 2022Review
- SARS-CoV-2-specific T cells associate with inflammation and reduced lung function in pulmonary post-acute sequalae of SARS-CoV-2.PLoS pathogens · 2022Article
- Elevated proportion of TLR2- and TLR4-expressing Th17-like cells and activated memory B cells was associated with clinical activity of cerebral cavernous malformations.Journal of neuroinflammation · 2022Article
- The Role of Ten-Eleven Translocation Proteins in Inflammation.Frontiers in immunology · 2022Review
- Review
- Effects of PD-1 blockade on ovarian follicles in a prepubertal female mouse.The Journal of endocrinology · 2021Article
- The Role of Immune Cells in Oxi-Inflamm-Aging.Cells · 2021Review
- Cancer risk in tuberculosis patients in a high endemic area.BMC cancer · 2021Article
- Host transcriptome response to Borrelia burgdorferi sensu lato.Ticks and tick-borne diseases · 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The strong association between specific alleles encoded within the MHC class II region and the development of rheumatoid arthritis (RA) has provided the best evidence to date that CD4+ T cells play a role in the pathogenesis of this chronic inflammatory disease. However, the unusual phenotype of synovial T cells, including their profound proliferative hyporesponsiveness to TCR ligation, has challenged the notion that T-cell effector responses are driven by cognate cartilage antigens in inflamed synovial joints. The hierarchy of T-cell dysfunction from peripheral blood to inflamed joint suggests that these defects are acquired through prolonged exposure to proinflammatory cytokines such as tumour necrosis factor (TNF)-alpha. Indeed, there are now compelling data to suggest that chronic cytokine activation may contribute substantially to the phenotype and effector function of synovial T cells. Studies reveal that chronic exposure of T cells to TNF uncouples TCR signal transduction pathways by impairing the assembly and stability of the TCR/CD3 complex at the cell surface. Despite this membrane-proximal effect, TNF selectively uncouples downstream signalling pathways, as is shown by the dramatic suppression of calcium signalling responses, while Ras/ERK activation is spared. On the basis of these data, it is proposed that T-cell survival and effector responses are driven by antigen-independent, cytokine-dependent mechanisms, and that therapeutic strategies that seek to restore T-cell homeostasis rather than further depress T-cell function should be explored in the future.
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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.