ArticleGenes2021
Altered Expression of TSPAN32 during B Cell Activation and Systemic Lupus Erythematosus.
Article in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Pooled it
- Transcriptomic and Clinical Profiling RevealsGenes · 2025Article
- TCF3 and ID3 Regulate TSPAN32 Expression in Burkitt Lymphoma.Scandinavian journal of immunology · 2025Article
- Comprehensive Analysis of TSPAN32 Regulatory Networks and Their Role in Immune Cell Biology.Biomolecules · 2025Article
- Innovative Phospholipid Carriers: A Viable Strategy to Counteract Antimicrobial Resistance.International journal of molecular sciences · 2023Review
- TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN.Signal transduction and targeted therapy · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease with various clinical features. Autoreactive B cells play a role in disease pathogenesis, through the production of multiple autoantibodies, which form immune complexes and induce the inflammatory response and tissue damage associated with SLE. Recently, tetraspanins, and in particular, TSPAN32, have been recognized to play a central role in immunity, as they are involved in various biological processes, such as the antigen presentation and the activation of lymphocytes. Evidence suggests that tetraspanins could represent in the future a target for therapeutic purposes in patients suffering from autoimmune/immunoinflammatory disorders. In the present study, by performing in silico analyses of high-throughput data, we evaluated the expression levels of TSPAN32 in B cell activation and investigated its modulation in circulating B cells from SLE patients. Our data show that B cell activation is associated with a significant downregulation of TSPAN32. Additionally, significantly lower levels of TSPAN32 were observed in circulating plasmablasts from SLE patients as compared to healthy donor plasmablasts. In addition, type I interferons (IFNs)-related genes were enriched among the genes negatively correlated to TSPAN32, in SLE plasmablasts. Accordingly, IFN-α is able to induce a dose-dependent downregulation of TSPAN32 in B cells. Overall, the data here presented suggest the potential use of TSPAN32 as a diagnostic marker and therapeutic target for the evaluation and management of humoral immune responses in chronic diseases, such as SLE.
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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.