ArticleLupus science & medicine2016
Characterisation of an epigenetically altered CD4(+) CD28(+) Kir(+) T cell subset in autoimmune rheumatic diseases by multiparameter flow cytometry.
Article in Lupus science & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Deciphering the role of SNP variants of co-stimulatory genes in systemic lupus erythematosus: from genotype to protein expression.BMC immunology · 2026Article
- Flavonoids Activation of the Transcription Factor Nrf2 as a Hypothesis Approach for the Prevention and Modulation of SARS-CoV-2 Infection Severity.Antioxidants (Basel, Switzerland) · 2020Article
- Epigenetic dysregulation of ACE2 and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients.Clinical immunology (Orlando, Fla.) · 2020Article
- Article
- Review
- New insights into the genetics and epigenetics of systemic sclerosis.Nature reviews. Rheumatology · 2018Review
- DNA methylation 101: what is important to know about DNA methylation and its role in SLE risk and disease heterogeneity.Lupus science & medicine · 2018Article
- Deoxyribonucleic Acid Methylation in Systemic Lupus Erythematosus: Implications for Future Clinical Practice.Frontiers in immunology · 2018Review
- CD4+CD28+KIR+CD11aJournal of autoimmunity · 2018Article
- Oxidative T Cell Modifications in Lupus and Sjogren's Syndrome.Lupus (Los Angeles) · 2017Article
- Protein Phosphatase 5 Contributes to the Overexpression of Epigenetically Regulated T-Lymphocyte Genes in Patients with Lupus.Lupus (Los Angeles) · 2016Article
- Functionally Diverse NK-Like T Cells Are Effectors and Predictors of Successful Aging.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesAntigen-specific CD4(+) T cells epigenetically modified with DNA methylation inhibitors overexpress genes normally suppressed by this mechanism, including CD11a, CD70, CD40L and the KIR gene family. The altered cells become autoreactive, losing restriction for nominal antigen and responding to self-class II major histocompatibility complex (MHC) molecules without added antigen, and are sufficient to cause a lupus-like disease in syngeneic mice. T cells overexpressing the same genes are found in patients with active lupus. Whether these genes are co-overexpressed on the same or different cells is unknown. The goal of this study was to determine whether these genes are overexpressed on the same or different T cells and whether this subset of CD4(+) T cells is also present in patients with lupus and other rheumatic diseases.
methodsMulticolour flow cytometry was used to compare CD11a, CD70, CD40L and KIR expression on CD3(+)CD4(+)CD28(+) T cells to their expression on experimentally demethylated CD3(+)CD4(+)CD28(+) T cells and CD3(+)CD4(+)CD28(+) T cells from patients with active lupus and other autoimmune diseases.
resultsExperimentally demethylated CD4(+) T cells and T cells from patients with active lupus have a CD3(+)CD4(+)CD28(+)CD11a(hi)CD70(+)CD40L(hi)KIR(+) subset, and the subset size is proportional to lupus flare severity. A similar subset is found in patients with other rheumatic diseases including rheumatoid arthritis, systemic sclerosis and Sjögren's syndrome but not retroperitoneal fibrosis.
conclusionsPatients with active autoimmune rheumatic diseases have a previously undescribed CD3(+)CD4(+)CD28(+)CD11a(hi)CD70(+)CD40L(hi)KIR(+) T cell subset. This subset may play an important role in flares of lupus and related autoimmune rheumatic diseases, provide a biomarker for disease activity and serve as a novel therapeutic target for the treatment of lupus flares.
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