ReviewAutoimmunity2010
Systems biology of lupus: mapping the impact of genomic and environmental factors on gene expression signatures, cellular signaling, metabolic pathways, hormonal and cytokine imbalance, and selecting targets for treatment.
Review in Autoimmunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 64 citations in OpenAlex.
- Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- T-Cell Immunosenescence in Systemic Lupus Erythematosus: Molecular Mechanisms and Therapeutic Perspectives.Clinical reviews in allergy & immunology · 2026Review
- Urinary 8-oxoGuo as a potential novel evaluation biomarker for patients with systemic lupus erythematosus.Clinical and experimental medicine · 2025Article
- Review
- Breaking the cycle: immune complexes, complement activation, and novel immunotherapies in lupus nephritis.Frontiers in immunology · 2025Review
- Article
- Redox Pathogenesis in Rheumatic Diseases.ACR open rheumatology · 2024Review
- Principles behind SLE treatment withImmunometabolism (Cobham, Surrey) · 2022Review
- Redox Control of Integrin-Mediated Hepatic Inflammation in Systemic Autoimmunity.Antioxidants & redox signaling · 2022Review
- Perturbed autophagy intervenes systemic lupus erythematosus by active ingredients of traditional Chinese medicine.Frontiers in pharmacology · 2022Review
- Glycation end-products specific auto-antibodies in Systemic Lupus Erythematosus.Bioinformation · 2022Article
- Editorial: New biomarkers for the diagnosis and treatment of systemic lupus erythematosus.Frontiers in immunology · 2022Article
- Insufficient Iron Improves Pristane-Induced Lupus by Promoting Treg Cell Expansion.Frontiers in immunology · 2022Article
- Oxidative Stress in SLE T Cells, Is NRF2 Really the Target to Treat?Frontiers in immunology · 2021Review
- Lupus-associated endogenous retroviral LTR polymorphism and epigenetic imprinting promote HRES-1/RAB4 expression and mTOR activation.JCI insight · 2020Article
- Personalized therapy design for systemic lupus erythematosus based on the analysis of protein-protein interaction networks.PloS one · 2020Article
- TREX1 D18N mice fail to process erythroblast DNA resulting in inflammation and dysfunctional erythropoiesis.Autoimmunity · 2018Article
- Crosstalk between metabolism and epigenetic modifications in autoimmune diseases: a comprehensive overview.Cellular and molecular life sciences : CMLS · 2018Review
- Review: Metabolic Control of Immune System Activation in Rheumatic Diseases.Arthritis & rheumatology (Hoboken, N.J.) · 2017Review
- Oxidative Stress and Treg and Th17 Dysfunction in Systemic Lupus Erythematosus.Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is characterized by the dysfunction of T cells, B cells, and dendritic cells, the release of pro-inflammatory nuclear materials from necrotic cells, and the formation of antinuclear antibodies (ANA) and immune complexes of ANA with DNA, RNA, and nuclear proteins. Activation of the mammalian target of rapamycin (mTOR) has recently emerged as a key factor in abnormal activation of T and B cells in SLE. In T cells, increased production of nitric oxide and mitochondrial hyperpolarization (MHP) were identified as metabolic checkpoints upstream of mTOR activation. mTOR controls the expression T-cell receptor-associated signaling proteins CD4 and CD3zeta through increased expression of the endosome recycling regulator Rab5 and HRES-1/Rab4 genes, enhances Ca2+ fluxing and skews the expression of tyrosine kinases both in T and B cells, and blocks the expression of Foxp3 and the generation of regulatory T cells. MHP, increased activity of mTOR, Rab GTPases, and Syk kinases, and enhanced Ca2+ flux have emerged as common T and B cell biomarkers and targets for treatment in SLE.
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.