ArticleThe Journal of clinical investigation2005
T cell hyperactivity in lupus as a consequence of hyperstimulatory antigen-presenting cells.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
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
63 citing papers in PubMed, 120 citations in OpenAlex.
- Neutrophil Antigen Presentation Reprograms the Tumor Microenvironment and Elicits Durable and Broad Antitumor Immunity.Cancer research communications · 2026Article
- Review
- KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes.Communications biology · 2024Article
- Autoimmune Responses and Therapeutic Interventions for Systemic Lupus Erythematosus: A Comprehensive Review.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Lysosomes as a therapeutic target.Nature reviews. Drug discovery · 2019Review
- The cytokine network type I IFN-IL-27-IL-10 is augmented in murine and human lupus.Journal of leukocyte biology · 2019Article
- Novel Autoantibodies Related to Cell Death and DNA Repair Pathways in Systemic Lupus Erythematosus.Genomics, proteomics & bioinformatics · 2019Article
- Inhibition of fatty acid metabolism by etomoxir or TOFA suppresses murine dendritic cell activation without affecting viability.Immunopharmacology and immunotoxicology · 2019Article
- TLR7 Protein Expression in Mild and Severe Lupus-Prone Models Is Regulated in a Leukocyte, Genetic, and IRAK4 Dependent Manner.Frontiers in immunology · 2019Article
- A Model for Apoptotic-Cell-Mediated Adaptive Immune EvasionFrontiers in pharmacology · 2019Article
- Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus.Mediators of inflammation · 2018Review
- The Involvement of MicroRNAs in Modulation of Innate and Adaptive Immunity in Systemic Lupus Erythematosus and Lupus Nephritis.Journal of immunology research · 2018Review
- Dysregulated Lymphoid Cell Populations in Mouse Models of Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2017Review
- VISTA Deficiency Accelerates the Development of Fatal Murine Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- Antigen presenting cell abnormalities in the Cln3(-/-) mouse model of juvenile neuronal ceroid lipofuscinosis.Biochimica et biophysica acta · 2016Article
- Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis.Inflammation · 2016Article
- Alpha 1 Antitrypsin Inhibits Dendritic Cell Activation and Attenuates Nephritis in a Mouse Model of Lupus.PloS one · 2016Article
- Dendritic Cells in Systemic Lupus Erythematosus: From Pathogenic Players to Therapeutic Tools.Mediators of inflammation · 2016Review
- Genetic and cellular dissection of the activation of AM14 rheumatoid factor B cells in a mouse model of lupus.Journal of leukocyte biology · 2015Article
- Dysregulated CD4+ T cells from SLE-susceptible mice are sufficient to accelerate atherosclerosis in LDLr-/- mice.Annals of the rheumatic diseases · 2015Article
3 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
8 authors at 1 institution in 1 country.
Funding
Abstract
Sle3 is an NZM2410-derived lupus susceptibility locus on murine chromosome 7. Congenic recombination has resulted in a novel mouse strain, B6.Sle3, associated with serum antinuclear autoantibodies (ANAs), T cell hyperactivity, and elevated CD4/CD8 ratios. An OVA-specific TCR transgene was used as a tool to demonstrate that Sle3 facilitated heightened T cell expansion in vitro, and in vivo, following antigen challenge. Indeed, continued T cell expansion was noted even in response to a tolerogenic signal. However, these phenotypes did not appear to be T cell intrinsic but were dictated by hyperstimulatory B6.Sle3 APCs. Importantly, B6.Sle3-derived DCs and macrophages appeared to be significantly more mature/activated, less apoptotic, and more proinflammatory and were better at costimulating T cells in vitro, compared with the B6 counterparts. Finally, the adoptive transfer of B6.Sle3-derived DCs into healthy B6 recipients elicited increased CD4/CD8 ratios and serum ANAs, 2 cardinal Sle3-associated phenotypes. We posit that their heightened expression of various costimulatory molecules, including CD80, CD106, I-A, and CD40, and their elevated production of various cytokines, including IL-12 and IL-1beta, may explain why Sle3-bearing DCs may be superior at breaching self tolerance. These studies provide mechanistic evidence indicating that intrinsic abnormalities in DCs and possibly other myeloid cells may dictate several of the phenotypes associated with systemic lupus, including ANA formation and T cell hyperactivity.
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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.