ReviewInflammation2023
Role of T Cells in the Pathogenesis of Rheumatoid Arthritis: Focus on Immunometabolism Dysfunctions.
Review in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular mechanisms and risk factors in rheumatoid arthritis: a comprehensive review.Inflammopharmacology · 2026Pooled it
- CD27 Neutralization Attenuates Rheumatoid Arthritis by Suppressing.Biochemical genetics · 2026Article
- Metabolic challenges in rheumatoid arthritis: a translational overview from pathogenesis to patient care.Acta diabetologica · 2026Review
- Metabolic exhaustion and immune ageing in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- Targeting mitochondrial oxidative stress: A novel therapeutic strategy for degenerative joint diseases (Review).Biomedical reports · 2026Review
- Exploring the Shared Diagnostic Biomarkers and Molecular Mechanisms Related to Mitochondrial Dysfunction in Inflammatory Bowel Disease and Rheumatoid Arthritis.Current issues in molecular biology · 2026Article
- Immune regulation and cell metabolism in B cell subsets in patients with systemic lupus erythematosus.Frontiers in immunology · 2026Review
- The associations between nailfold microvascular abnormalities and systemic inflammation or Th17/Treg dysregulation in rheumatoid arthritis.Frontiers in immunology · 2026Observational
- Novel involvement of LMTK2 and EML6 in rheumatoid arthritis: potential biomarkers for disease activity and seronegative patients.Frontiers in immunology · 2026Article
- Dual-omics analysis of key biomarkers in T cell ubiquitination of rheumatoid arthritis blood and synovial tissue, validated by two-sample Mendelian randomization and qPCR.Frontiers in immunology · 2026Article
- Metabolic Reprogramming of T Cells by MSCs Rebalances Th17/Treg Axis to Attenuate Collagen-Induced Arthritis.Journal of immunology research · 2026Article
- The genetic puzzle of rheumatoid arthritis: Causes, progression, and treatment.Biochemistry and biophysics reports · 2025Review
- Neutrophils: a Central Point of Interaction Between Immune Cells and Nonimmune Cells in Rheumatoid Arthritis.Clinical reviews in allergy & immunology · 2025Review
- T Cell Dysregulation in Rheumatoid Arthritis: from Genetic Susceptibility to Established Disease.Current rheumatology reports · 2025Review
- The Role of Long Non-Coding RNA in Rheumatoid Arthritis.International journal of molecular sciences · 2025Review
- Biomaterials for Modulating the Immune Microenvironment in Rheumatoid Arthritis.BME frontiers · 2025Review
- Individualized diagnosis of rheumatoid arthritis: A rank-based qualitative T cell-related signature.PloS one · 2025Article
- Article
- Evaluation of hematological markers as prognostic tools in rheumatoid arthritis.BMC rheumatology · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence demonstrated that metabolic-associated T cell abnormalities could be detected in the early stage of RA development. In this context, molecular evaluations have revealed changes in metabolic pathways, leading to the aggressive phenotype of RA T cells. A growing list of genes is downregulated or upregulated in RA T cells, and most of these genes with abnormal expression fall into the category of metabolic pathways. It has been shown that RA T cells shunt glucose towards the pentose phosphate pathway (PPP), which is associated with a high level of nicotinamide adenine dinucleotide phosphate (NADPH) and intermediate molecules. An increased level of NADPH inhibits ATM activation and thereby increases the proliferation capabilities of the RA T cells. Defects in the DNA repair nuclease MRE11A cause failures in repairing mitochondrial DNA, resulting in inhibiting the fatty acid oxidation pathway and further elevated cytoplasmic lipid droplets. Accumulated lipid droplets employ to generate lipid membranes for the cell building program and are also used to form the front-end membrane ruffles that are accomplices with invasive phenotypes of RA T cells. Metabolic pathway involvement in RA pathogenesis expands the pathogenic concept of the disease beyond the common view of autoimmunity triggered by autoantigen recognition. Increased knowledge about metabolic pathways' implications in RA pathogenesis paves the way to understand better the environment/gene interactions and host/microbiota interactions and introduce potential therapeutic approaches. This review summarized emerging data about the roles of T cells in RA pathogenesis with a focus on immunometabolism dysfunctions and how these metabolic alterations can affect the disease process.
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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.