ArticleBrain sciences2020
Impaired Expression of Tetraspanin 32 (TSPAN32) in Memory T Cells of Patients with Multiple Sclerosis.
Article in Brain sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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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
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.
- Pooled it
- Pooled it
- Possible relationship between genetic polymorphisms and the risk of exercise addiction among Turkish elite athletes: an exploratory pilot study.Scientific reports · 2026Article
- Transcriptional Control of TSPAN32 in T-ALL Reveals Interplay Between TAL1 and NOTCH1.Biomedicines · 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
- The State of the Art of Pediatric Multiple Sclerosis.International journal of molecular sciences · 2023Review
- Review
- Transcriptomic Data Analysis Reveals a Down-Expression ofBrain sciences · 2021Article
- Altered Expression of TSPAN32 during B Cell Activation and Systemic Lupus Erythematosus.Genes · 2021Article
- Advances in Multiple Sclerosis Research-Series I.Brain sciences · 2020Article
- Transcriptomic Analysis Reveals Abnormal Expression of Prion Disease Gene Pathway in Brains from Patients with Autism Spectrum Disorders.Brain sciences · 2020Article
- Exploratory Analysis of iPSCS-Derived Neuronal Cells as Predictors of Diagnosis and Treatment of Alzheimer Disease.Brain sciences · 2020Article
- Emerging Role of the Macrophage Migration Inhibitory Factor Family of Cytokines in Neuroblastoma. Pathogenic Effectors and Novel Therapeutic Targets?Molecules (Basel, Switzerland) · 2020Review
- Rituximab Prevents the Development of Experimental Autoimmune Encephalomyelitis (EAE): Comparison with Prophylactic, Therapeutic or Combinational Regimens.Journal of inflammation research · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Tetraspanins are a conserved family of proteins involved in a number of biological processes. We have previously shown that Tetraspanin-32 (TSPAN32) is significantly downregulated upon activation of T helper cells via anti-CD3/CD28 stimulation. On the other hand, TSPAN32 is marginally modulated in activated Treg cells. A role for TSPAN32 in controlling the development of autoimmune responses is consistent with our observation that encephalitogenic T cells from myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mice exhibit significantly lower levels of TSPAN32 as compared to naïve T cells. In the present study, by making use of ex vivo and in silico analysis, we aimed to better characterize the pathophysiological and diagnostic/prognostic role of TSPAN32 in T cell immunity and in multiple sclerosis (MS). We first show that TSPAN32 is significantly downregulated in memory T cells as compared to naïve T cells, and that it is further diminished upon ex vivo restimulation. Accordingly, following antigenic stimulation, myelin-specific memory T cells from MS patients showed significantly lower expression of TSPAN32 as compared to memory T cells from healthy donors (HD). The expression levels of TSPAN32 was significantly downregulated in peripheral blood mononuclear cells (PBMCs) from drug-naïve MS patients as compared to HD, irrespective of the disease state. Finally, when comparing patients undergoing early relapses in comparison to patients with longer stable disease, moderate but significantly lower levels of TSPAN32 expression were observed in PBMCs from the former group. Our data suggest a role for TSPAN32 in the immune responses underlying the pathophysiology of MS and represent a proof-of-concept for additional studies aiming at dissecting the eventual contribution of TSPAN32 in other autoimmune diseases and its possible use of TSPAN32 as a diagnostic factor and therapeutic target.
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