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T Lymphocyte Serotonin 5-HT 7 Receptor Is Dysregulated in Natalizumab-Treated Multiple Sclerosis Patients.
- Source :
- Biomedicines; Oct2022, Vol. 10 Issue 10, pN.PAG-N.PAG, 12p
- Publication Year :
- 2022
-
Abstract
- Serotonin (5-HT) is known as a potent immune cell modulator in autoimmune diseases and should be protective in the pathogenesis of multiple sclerosis (MS). Nevertheless, there is limited knowledge about receptors involved in 5-HT effects as well as induced mechanisms. Among 5-HT receptors, the 5-HT<subscript>7</subscript> receptor is able to activate naïve T cells and influence the inflammatory response; however, its involvement in the disease has never been studied so far. In this study, we collected blood sample from three groups: acute relapsing MS patients (ARMS), natalizumab-treated MS patients (NTZ), and control subjects. We investigated the 5-HT<subscript>7</subscript> expression on circulating lymphocytes and evaluated the effects of its activation on cytokine production with peripheral blood mononuclear cell (PBMC) cultures. We found a significant increase in the 5-HT<subscript>7</subscript> surface expression on T lymphocytes and on the different CD4<superscript>+</superscript> T cell subsets exclusively in NTZ-treated patients. We also showed that the selective agonist 5-carboxamidotryptamine (5-CT)-induced 5-HT<subscript>7</subscript>R activation significantly promotes the production of IL-10, a potent immunosuppressive cytokine in PBMCs. This study provides for the first time a dysregulation of 5-HT<subscript>7</subscript> expression in NTZ-MS patients and its ability to promote IL-10 release, suggesting its protective role. These findings strengthen the evidence that 5-HT<subscript>7</subscript> may play a role in the immuno-protective mechanisms of NTZ in MS disease and could be considered as an interesting therapeutic target in MS. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 22279059
- Volume :
- 10
- Issue :
- 10
- Database :
- Complementary Index
- Journal :
- Biomedicines
- Publication Type :
- Academic Journal
- Accession number :
- 159870499
- Full Text :
- https://doi.org/10.3390/biomedicines10102418