Peripheral helper T cells in the pathogenesis of multiple sclerosis. (August 2022)

• Record Type: Journal Article
• Authors: Holm Hansen, Rikke; Højsgaard Chow, Helene; Talbot, Jacob; Buhelt, Sophie; Nickelsen Hellem, Marie Nathalie; Nielsen, Jørgen Erik; Sellebjerg, Finn Thorup; von Essen, Marina Rode
• Is Part Of: Multiple sclerosis. Volume 28:Number 9(2022)
• Page Start: 1340
• Page End: 1350
• Publication Date: 2022-08
• Subjects: Multiple sclerosis -- peripheral helper T cells -- immunosurveillance -- immunology -- intrathecal antibody production -- multiple sclerosis pathogenesis; Central nervous system -- Diseases -- Periodicals; Myelin sheath -- Diseases -- Periodicals; Inflammation -- Periodicals; Multiple sclerosis -- Periodicals; Central Nervous System Diseases -- Periodicals; Demyelinating Diseases -- Periodicals; Inflammation -- Periodicals; Multiple Sclerosis -- Periodicals; Système nerveux central -- Maladies -- Périodiques; Gaine de myéline -- Maladies -- Périodiques; Inflammation (Pathologie) -- Périodiques; Sclérose en plaques -- Périodiques; Electronic journals; 616.834005
• DOI: 10.1177/13524585211067696
• Languages: English
• ISSNs: 1352-4585

Abstract

Background: Peripheral helper T cells (Tph) are likely implicated in the pathogenesis of various inflammatory diseases. Tph cells share functions with follicular helper T cells, including plasma cell differentiation and antibody production. Objective and methods: To investigate a possible role of Tph cells in the pathogenesis of multiple sclerosis (MS), we used flow cytometry to analyze the function, phenotype, and central nervous system (CNS)-recruitment of Tph cells in the blood and cerebrospinal fluid (CSF) from controls and patients with relapsing–remitting (RR) and primary progressive (PP) MS. Result: This study identified two functionally distinct Tph cell populations and a regulatory counterpart, Tpr cells. No differences in blood frequencies, cytokine production, or potential to interact with B cells were found between controls and patients with MS. Along with an equal CNS-migration potential, we found both Tph cell populations enriched in the CSF; and surprisingly, an increased frequency of intrathecal Tph cells in the control group compared to patients with MS. Conclusion: Altogether, we did not find an increased frequency of CSF Tph cells in patients with RRMS or PPMS. Our findings indicate that rather than being involved in MS pathogenesis, Tph cells may be implicated in normal CNS immunosurveillance.