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Comparison of OX40 expression in patients with multiple sclerosis and neuromyelitis optica as an approach to diagnosis

Authors :
Mostafa Manian
Morteza Motallebnezhad
Reza Nedaeinia
Rasoul Salehi
Leila Khani
Gordon A. Ferns
Mir Hadi Jazayeri
Source :
Allergy, Asthma & Clinical Immunology, Vol 19, Iss 1, Pp 1-8 (2023)
Publication Year :
2023
Publisher :
BMC, 2023.

Abstract

Abstract Background Previous studies have shown that CD134 (OX40) co-stimulation is involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) models and the antigen is expressed within multiple sclerosis lesions in humans. OX40 (CD134) is thought to be a secondary co-stimulatory immune checkpoint molecule that is expressed by T cells. This study aimed to evaluate the mRNA expression of OX40 and its serum levels in the peripheral blood of patients with Multiple Sclerosis (MS) or Neuromyelitis Optica (NMO). Methods Patients with MS (n = 60), NMO (n = 20), and 20 healthy subjects were recruited from Sina Hospital, Tehran, Iran. The diagnoses were confirmed by a specialist in clinical neurology. Peripheral venous blood was obtained from all subjects, and mRNA quantification of OX40 was conducted using real-time PCR. Serum samples were also obtained and the concentration of OX40 was determined using an enzyme-linked immunosorbent assay (ELISA). Results There was a significant correlation between the mRNA expression and serum levels of OX40 and disability as assessed using the expanded disability status scale (EDSS) in the patients with MS, but not in the patients with NMO. Expression of OX40 mRNA was significantly higher in the peripheral blood of MS patients compared to healthy individuals and NMO patients (*P

Details

Language :
English
ISSN :
17101492
Volume :
19
Issue :
1
Database :
Directory of Open Access Journals
Journal :
Allergy, Asthma & Clinical Immunology
Publication Type :
Academic Journal
Accession number :
edsdoj.4730bbae08d3429f8ad86129dda613b2
Document Type :
article
Full Text :
https://doi.org/10.1186/s13223-023-00772-9