Loading…

Increased expression of PD-1 in CD8 + CD3 + T cells correlates with EBV viral load in MS patients

Multiple sclerosis (MS) is one of the common autoimmune diseases. The exact etiology of MS is still unclear, but recent studies have shown the possibility of infectious agent involvement such as Epstein-Barr virus (EBV) in MS pathophysiology. In this study, CD3  +  CD8  +  T cells of 25 new case MS...

Full description

Saved in:
Bibliographic Details
Published in:Journal of neurovirology 2022-12, Vol.28 (4-6), p.497-504
Main Authors: Najmadini, Atefeh, Mohammadi, Mohammad Mahdi, Langroudi, Ladan, Meimand, Hosseinali Ebrahimi, Mahmoodi, Merat, Mirzaei, Moghadameh
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Multiple sclerosis (MS) is one of the common autoimmune diseases. The exact etiology of MS is still unclear, but recent studies have shown the possibility of infectious agent involvement such as Epstein-Barr virus (EBV) in MS pathophysiology. In this study, CD3  +  CD8  +  T cells of 25 new case MS patients were compared with healthy donors for expression of exhaustion marker, PD-1, using flow cytometry. Also, the expression of the EBV gene, BRCF-1, in PBMCs was analyzed using real-time PCR. Results revealed a lower frequency of CD3  +  CD8  +  T cells in MS patients. Also, increased expression of PD-1 was observed on CTLs which correlated with higher viral loads. Therefore, a lower frequency of CD8  +  T cells but a higher exhaustion marker in MS patients reveals a new mechanism of EBV pathogenesis in MS development. The results suggest that inefficient immune control of EBV in patients with MS may cause exacerbation of the disease. Future studies on the mechanism of T cell exhaustion and chronic infections may aid in a better understanding of the disease and the design of effective therapies.
ISSN:1355-0284
1538-2443
DOI:10.1007/s13365-022-01083-2