ArticleThe Journal of clinical investigation2018
Kidney-infiltrating T cells in murine lupus nephritis are metabolically and functionally exhausted.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
What it found
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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.
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Who cites it
105 citing papers in PubMed, 144 citations in OpenAlex.
- Discovery of Post-Translationally Modified Epitopes in Autoimmunity: Someone Has to Fish so Everyone Can Eat.Immunological reviews · 2026Review
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- CD8MedComm · 2026Review
- Article
- Peripheral and renal interstitial T-cell profiles associated with treatment response in lupus nephritis: a retrospective cohort study.Clinical kidney journal · 2026Article
- The CD8 immgenT framework as a universal reference of mouse CD8αβ T cell differentiation states.bioRxiv : the preprint server for biology · 2026Article
- Type I interferon drives dysfunction of a distinct CD8+ HLA-DRB1+ T cell subset in systemic lupus erythematosus.medRxiv : the preprint server for health sciences · 2026Article
- CD8Frontiers in immunology · 2026Review
- Checkpoint-enriched T cells with retained effector-associated features are associated with disease activity in systemic lupus erythematosus.Frontiers in immunology · 2026Article
- Harnessing tumor immune checkpoints for autoimmune disease therapeutics.Frontiers in immunology · 2026Review
- Lymphocyte activation gene 3 in autoimmune disease: from molecular mechanisms to clinical applications.Frontiers in immunology · 2026Review
- Revitalizing T cells: breakthroughs and challenges in overcoming T cell exhaustion.Signal transduction and targeted therapy · 2026Review
- Single-cell Unperturbed Activation Profiling by mass cytometry capturesFrontiers in immunology · 2026Article
- Immunopathogenesis and Therapeutics of Systemic Lupus Erythematosus: an Integrative Review.Clinical reviews in allergy & immunology · 2025Review
- Pathogenic drivers of lupus myocarditis and potential therapeutic targets.Experimental & molecular medicine · 2025Review
- Cytotoxic Molecules as Potential Biomarkers for Active and Inactive Systemic Lupus Erythematosus.Biomedicines · 2025Article
- Alterations in genes associated with cytosolic RNA sensing in whole blood are associated with coronary microvascular disease in SLE.Scientific reports · 2025Article
- Metabolic reprogramming as a therapeutic target for modulating the Th17/Treg balance in autoimmune diseases: a comprehensive review.Frontiers in immunology · 2025Review
- PD-1 activation mitigates lupus nephritis by suppressing hyperactive and heterogeneous PD-1Theranostics · 2025Article
- Tissue-resident memory T cells in urinary tract diseases.Frontiers in immunology · 2025Review
45 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
9 authors at 2 institutions in 2 countries.
Funding
Abstract
While T cells are important for the pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis, little is known about how T cells function after infiltrating the kidney. The current paradigm suggests that kidney-infiltrating T cells (KITs) are activated effector cells contributing to tissue damage and ultimately organ failure. Herein, we demonstrate that the majority of CD4+ and CD8+ KITs in 3 murine lupus models are not effector cells, as hypothesized, but rather express multiple inhibitory receptors and are highly dysfunctional, with reduced cytokine production and proliferative capacity. In other systems, this hypofunctional profile is linked directly to metabolic and specifically mitochondrial dysfunction, which we also observed in KITs. The T cell phenotype was driven by the expression of an "exhausted" transcriptional signature. Our data thus reveal that the tissue parenchyma has the capability of suppressing T cell responses and limiting damage to self. These findings suggest avenues for the treatment of autoimmunity based on selectively exploiting the exhausted phenotype of tissue-infiltrating T cells.
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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.