ReviewJournal of immunology research2014
The pathology of T cells in systemic lupus erythematosus.
Review in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Systemic Lupus Erythematosus and DNA Degradation and Elimination Defects.Frontiers in immunology · 2019Pooled it
- Circulating miR-320b Contributes to CD4+ T-Cell Proliferation in Systemic Lupus Erythematosus via MAP3K1.Journal of immunology research · 2023Trial
- Immunopathogenesis of neuropsychiatric systemic lupus erythematosus: current insights into inflammatory and thrombotic pathways.Journal of neuroinflammation · 2026Review
- Persistent cutaneous lupus erythematosus: A pathway toward systemic disease?Journal of translational autoimmunity · 2026Review
- Review
- Functional DNA Repair Profiling in Translational Medicine: Benchmarking Comet, γH2AX, and NGS Assays Against Clinical Constraints.Current issues in molecular biology · 2026Review
- Immunopathogenesis and Therapeutics of Systemic Lupus Erythematosus: an Integrative Review.Clinical reviews in allergy & immunology · 2025Review
- C1q Binds to CD4+ T Cells and Inhibits the Release of Pro-Inflammatory Cytokines: Role in the Pathogenesis of Systemic Lupus Erythematosus.International journal of molecular sciences · 2025Article
- IL-8/CD181 Mediated Inflammation in SLE-Associated Hemolytic Anemia.Iranian journal of pathology · 2025Article
- KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes.Communications biology · 2024Article
- T cell expressions of aberrant gene signatures and Co-inhibitory receptors (Co-IRs) as predictors of renal damage and lupus disease activity.Journal of biomedical science · 2024Article
- Emerging treatment for Sjögren's disease: a review of recent phase II and III trials.Expert opinion on emerging drugs · 2023Review
- Cutaneous Lupus Erythematosus: An Update on Pathogenesis and Future Therapeutic Directions.American journal of clinical dermatology · 2023Review
- mMolecular medicine (Cambridge, Mass.) · 2023Article
- Methylation ofDiagnostics (Basel, Switzerland) · 2022Article
- Dysregulation of immunity in COVID-19 and SLE.Inflammopharmacology · 2022Review
- An Overview of Systemic Lupus Erythematosus (SLE) Pathogenesis, Classification, and Management.Cureus · 2022Review
- Role of the innate and adaptive immune responses in the pathogenesis of systemic lupus erythematosus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- T Cells, Interleukin-2 and Systemic Lupus Erythematosus-From Pathophysiology to Therapy.Cells · 2022Review
- Coexistence of Discoid Lupus Erythematosus and Paraneoplastic Pemphigus: A Case Report and Literature Review.Clinical, cosmetic and investigational dermatology · 2022Article
27 more citing papers are in PubMed but not listed here.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is characterized by the production of a wide array of autoantibodies. Thus, the condition was traditionally classified as a "B-cell disease". Compelling evidence has however shown that without the assistance of the helper T lymphocytes, it is indeed difficult for the "helpless" B cells to become functional enough to trigger SLE-related inflammation. T cells have been recognized to be crucial in the pathogenicity of SLE through their capabilities to communicate with and offer enormous help to B cells for driving autoantibody production. Recently, a number of phenotypic and functional alterations which increase the propensity to trigger lupus-related inflammation have been identified in lupus T cells. Here, potential mechanisms involving alterations in T-cell receptor expressions, postreceptor downstream signalling, epigenetics, and oxidative stress which favour activation of lupus T cells will be discussed. Additionally, how regulatory CD4+, CD8+, and γδ T cells tune down lupus-related inflammation will be highlighted. Lastly, while currently available outcomes of clinical trials evaluating therapeutic agents which manipulate the T cells such as calcineurin inhibitors indicate that they are at least as efficacious and safe as conventional immunosuppressants in treating lupus glomerulonephritis, larger clinical trials are undoubtedly required to validate these as-yet favourable findings.
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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.