ReviewCurrent opinion in immunology2017
Metabolic signatures of T-cells and macrophages in rheumatoid arthritis.
Review in Current opinion in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed.
- Identification of Diagnostic Biomarkers Among Metabolism-related Genes in Rheumatoid Arthritis: Insights into Immune Landscape and Molecular Subtype Characterization.Applied biochemistry and biotechnology · 2026Article
- Metabolic exhaustion and immune ageing in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Gene Expression Alterations in Peripheral Blood Mononuclear Cells and Cartilage Explants from End-Stage Rheumatoid Arthritis Patients in Response to Taurine: A Pilot Exploratory Study.Life (Basel, Switzerland) · 2026Article
- Mitochondria as an Integrative Hub of Cellular Homeostasis and Stress Response.International journal of molecular sciences · 2026Review
- Untargeted metabolomics reveals immune-metabolic signatures in established cases of rheumatoid arthritis.Frontiers in molecular biosciences · 2026Article
- Fatty Acid Metabolic Reprogramming in Rheumatoid Arthritis: Integrating Inflammation, Resolution Failure, and Joint Destruction.Journal of inflammation research · 2026Review
- Immune remodeling and metabolic reprogramming in chronic fatigue: insights into GPCR signaling and epigenetic regulation.Frontiers in immunology · 2026Review
- Trained Immunity Exacerbates Inflammatory Arthritis Progression via Promoting Synovial Fibroblast Ferroptotic Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Lactate signalling leads to aggregation of immune-inflammatory hotspots and SLC5A12 blockade promotes their resolution.Nature metabolism · 2025Article
- Immune Aging in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Review
- Combination strategies of gut microbiota in cancer therapy through metabolic reprogramming and immune remodeling.Cell communication and signaling : CCS · 2025Review
- SIRT3 deficiency reduces PFKFB3-driven T-cell glycolysis and promotes arthritic inflammation.Science China. Life sciences · 2025Article
- Mapping metabolic dependences and capacities using ATP as a biomarker.Research square · 2025Article
- Tumor Microenvironment Lactate: Is It a Cancer Progression Marker, Immunosuppressant, and Therapeutic Target?Molecules (Basel, Switzerland) · 2025Review
- Metabolic checkpoints in rheumatoid arthritis.Seminars in arthritis and rheumatism · 2025Review
- The small molecule inhibitor 3PO is a modulator of neutrophil metabolism, ROS production, and NET release.Clinical and experimental immunology · 2025Article
- Downregulated MYL1 Emerges as a Promising Diagnostic Biomarker for Rheumatoid Arthritis.Journal of inflammation research · 2025Article
- Deciphering Immunometabolic Landscape in Rheumatoid Arthritis: Integrative Multiomics, Explainable Machine Learning and Experimental Validation.Journal of inflammation research · 2025Article
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
3 authors.
Funding
Abstract
In most autoimmune diseases, a decade-long defect in self-tolerance eventually leads to clinically relevant, tissue-destructive inflammatory disease. The pathogenic potential of chronic persistent immune responses during the pre-clinical and clinical phase is ultimately linked to the bioenergetic fitness of innate and adaptive immune cells. Chronic immune cell stimulation, high cellular turn-over, structural damage to the host tissue and maladaptive wound healing, all require a reliable supply of nutrients, oxygen, and biosynthetic precursors. Here, we use the model system of rheumatoid arthritis (RA) to discuss immunometabolism from the vantage point of T-cells and macrophages that encounter fundamentally different metabolic stress scenarios in the RA host. We outline the general principle that both insufficient nutrient supply, as well as nutrient excess generate cellular stress responses and guide immune function. ATP
Indexed as
Identifiers
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.