ArticlePloS one2015
CD8+ T Cells Specific to Apoptosis-Associated Antigens Predict the Response to Tumor Necrosis Factor Inhibitor Therapy in Rheumatoid Arthritis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Lymphocytes as Biomarkers of Therapeutic Response in Rheumatic Autoimmune Diseases, Is It a Realistic Goal?Clinical reviews in allergy & immunology · 2017Pooled it
- HLA class I-naturally presented synovial tissue peptides are recognized by CD8+ T lymphocytes from rheumatoid arthritis patients.Frontiers in immunology · 2026Article
- Characteristics of the (Auto)Reactive T Cells in Rheumatoid Arthritis According to the Immune Epitope Database.International journal of molecular sciences · 2023Review
- Gene Ontology Analysis Highlights Biological Processes Influencing Non-Response to Anti-TNF Therapy in Rheumatoid Arthritis.Biomedicines · 2022Article
- Intersection Between Large Granular Lymphocyte Leukemia and Rheumatoid Arthritis.Frontiers in oncology · 2022Review
- Immune cell profiles in synovial fluid after anterior cruciate ligament and meniscus injuries.Arthritis research & therapy · 2021Article
- Validation of a Bioassay for Predicting Response to Tumor Necrosis Factor Inhibitors in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- T Cell Memory in Infection, Cancer, and Autoimmunity.Frontiers in immunology · 2021Review
- Combination of chemotherapy and PD-1 blockade induces T cell responses to tumor non-mutated neoantigens.Communications biology · 2020Article
- Using the Immunophenotype to Predict Response to Biologic Drugs in Rheumatoid Arthritis.Journal of personalized medicine · 2019Review
- Hepatitis E Virus (HEV)-Specific T Cell Receptor Cross-Recognition: Implications for Immunotherapy.Frontiers in immunology · 2019Article
- Article
- Leveraging blood and tissue CD4+ T cell heterogeneity at the single cell level to identify mechanisms of disease in rheumatoid arthritis.Current opinion in immunology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD8+ T cells specific to caspase-cleaved antigens derived from apoptotic T cells (apoptotic epitopes) represent a principal player in chronic immune activation, which is known to amplify immunopathology in various inflammatory diseases. The purpose of the present study was to investigate the relationship involving these autoreactive T cells, the rheumatoid arthritis immunopathology, and the response to tumor necrosis factor-α inhibitor therapy. The frequency of autoreactive CD8+ T cells specific to various apoptotic epitopes, as detected by both enzyme-linked immunospot assay and dextramers of major histocompatibility complex class I molecules complexed with relevant apoptotic epitopes, was longitudinally analyzed in the peripheral blood of rheumatoid arthritis patients who were submitted to etanercept treatment (or other tumor necrosis factor inhibitors as a control). The percentage of apoptotic epitope-specific CD8+ T cells was significantly higher in rheumatoid arthritis patients than in healthy donors, and correlated with the disease activity. More important, it was significantly more elevated in responders to tumor necrosis factor-α inhibitor therapy than in non-responders before the start of therapy; it significantly dropped only in the former following therapy. These data indicate that apoptotic epitope-specific CD8+ T cells may be involved in rheumatoid arthritis immunopathology through the production of inflammatory cytokines and that they may potentially represent a predictive biomarker of response to tumor necrosis factor-α inhibitor therapy to validate in a larger cohort of patients.
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