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Updated: Dec 30, 2025
Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Impaired Expression of Tetraspanin 32 (TSPAN32) in Memory T Cells of Patients with Multiple Sclerosis
Maria Sofia Basile1, Emanuela Mazzon2, Katia Mangano1
1Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123 Catania, Italy.
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.
Insights
Tetraspanin-32 (TSPAN32) is significantly downregulated in T cells of multiple sclerosis patients, suggesting its role in autoimmune disease pathology and potential as a diagnostic marker.
Area of Science:
- Immunology
- Molecular Biology
- Neuroscience
Background:
- Tetraspanins are proteins involved in various biological processes.
- Tetraspanin-32 (TSPAN32) is downregulated in activated T helper cells.
- TSPAN32 levels are lower in T cells from experimental autoimmune encephalomyelitis (EAE) models.
Purpose of the Study:
- To investigate the role of TSPAN32 in T cell immunity and multiple sclerosis (MS).
- To explore TSPAN32's potential as a diagnostic and prognostic factor in MS.
Main Methods:
- Ex vivo and in silico analysis of TSPAN32 expression.
- Comparison of TSPAN32 levels in T cells from MS patients and healthy donors (HD).
- Analysis of TSPAN32 expression in different disease states and during relapses.
Main Results:
- TSPAN32 is downregulated in memory T cells compared to naïve T cells and further reduced upon restimulation.
- Myelin-specific memory T cells from MS patients show lower TSPAN32 expression than those from HD.
- Peripheral blood mononuclear cells (PBMCs) from drug-naïve MS patients exhibit reduced TSPAN32 levels compared to HD.
- Patients with early relapses show lower TSPAN32 expression in PBMCs than those with stable disease.
Conclusions:
- TSPAN32 plays a role in the immune responses underlying MS pathophysiology.
- TSPAN32 may serve as a diagnostic factor and therapeutic target for MS and other autoimmune diseases.
