Abstract

Neuromyelitis optica (NMO), also known as Devic's disease, is an autoimmune disorder of the central nervous system (CNS) in which immune system cells and antibodies primarily attack the optic nerves and the spinal cord. OX40 (CD134) is a tumor necrosis factor (TNF)-receptor family member expressed primarily on activated CD4+ and CD8+ T-cells. In an autoimmune disease, OX40 is typically up-regulated at sites of inflammation, and increases in the number of peripheral CD4+ T-cells expressing OX40. OX40 and its ligand OX40L are key TNF members that augment T-cell expansion, cytokine production, and promote T-cell survival. The aim of this study was to evaluate and compare of OX40 gene expression and its serum levels in patients with NMO and healthy controls. Twenty sex-/age-matched healthy controls (HC) (median age = 32 years, 15 females/5 males) were engaged for the present study. Expression of OX40 at the transcript level and serum protein levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assays, respectively. The results indicated OX40 expression in patients was significantly lower than in healthy controls (p = 0.001). However, the serum level of OX40 was not significantly different between groups (p = 0.37). In addition, the results indicated that CD134 expression was not age-related (p = 0.041). Overall, this study suggests to us that OX40 levels are not a suitable marker for diagnosis or treatment of NMO.

Highlights

  • IntroductionOX40 is typically Introduction up-regulated at sites of inflammation, and increases in the number of peripheral CD4+ T-cells expressing OX40

  • OX40 mRNA in the white blood cells of Neuromyelitis optica (NMO) patients was found to be significantly (p = 0.001) lower than in control individuals’ cells

  • There appeared to be no correlation between OX40 mRNA and age in this group of NMO patients

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Summary

Introduction

OX40 is typically Introduction up-regulated at sites of inflammation, and increases in the number of peripheral CD4+ T-cells expressing OX40. Pair (see [1 compare of OX40 gene expression and its serum leAve,lAs ∗inis sLaiikde tmoubletipsleelfs-cdleuraolswish(MenSe),vNeMr tOheisrea reexliasptsinagn-raeumtiotmtinogrphism of th patients with NMO and healthy controls. Twenty sesxw-/agpes- A adnisdeaAse∗.[I1n, 2th].isDcuarisnegsuanchy arenlaapusteo,mnoewrphdiasmmagiseutnoiqthuee, and called matched healthy controls (HC) For i 15 females/5 males) were engaged for the presentastteuddwy.ithdaisnaibrirleitdy.uUcinblilkeemMoSd,uthleerfeoristhnoe Tperorgwrielslsigiveerpahlgaesberoaf othfitshe hypercub Expression of OX40 at the transcript level and Lseeorunmard pdaisieraosfeK. Trahwertecfhoroeu, kprteyvpeen(tisnegea[1tt0a,cDkseisncirtiitoicnal6t.1o])a;g(ioioi)dthe Leonard ppimroolmytemuinneoralseosverebcleshnawtianesrrseeaaymcste,iaroesnsup(rqeecRdtTivb-PeyClyRq. u)Tahannetdrietaesntuizvltyesmirneedmba-lilric-noataikdtm(eeusddeeleef[olp1ora,nttTgiheAh-entemetTorsome,rner>wgom7ui0N]tl,%clMio[g3Omae,rreTae.anhcldgehoeaNbrrMaercmaOteosrsfi4pza.ee1cdd,ti5rbsu.ty5ma]an);dcp(eirisev-ors)eredagnenucrelaa(oNprfpMgsrreOoarSppuDrmhi)athtealyt hnaosrma sap OX40 expression in patients was significantly lowe(srethea[n11, Laeumtomanati1b4o.d8i]e);s (avg)atinhset Lasetoroncayrtde wpaaitrerccohnasninsteilnagquoaf paonryintwo of a mod in healthy controls (p = 0.001). The results indicated thateCxDa1m34plessp(ieici)i,fi(civT)-acreellsspleikceialyl cpaasretsicoipfa(tve).in the pathogenesis

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