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Tumor necrosis factor alpha (TNF-α) and its soluble receptors are associated with disability, disability progression and clinical forms of multiple sclerosis.

Authors :
Ribeiro, Claudia Mara
Oliveira, Sayonara Rangel
Alfieri, Daniela Frizon
Flauzino, Tamires
Kaimen-Maciel, Damacio Ramón
Simão, Andréa Name Colado
Maes, Michael
Reiche, Edna Maria Vissoci
Source :
Inflammation Research. Dec2019, Vol. 68 Issue 12, p1049-1059. 11p.
Publication Year :
2019

Abstract

Background: The association between tumor necrosis factor (TNF)-α, soluble TNF receptor (sTNFR)1 and sTNFR2 with clinical characteristics of multiple sclerosis (MS) remains unclear. Objective: To examine whether TNF-α, sTNFR1 and sTNFR2 are associated with MS diagnosis, disability, disability progression and clinical forms of MS. Materials and subjects: The study included 147 patients with relapsing–remitting MS (RRMS), 21 with progressive clinical forms (ProgMS) and 70 controls. Expanded Disability Status Scale (EDSS) evaluated disability as mild (EDSS < 3.0) or moderate/high (EDSS ≥ 3.0). Multiple Sclerosis Severity Score (MSSS) evaluated disability progression as no progression (MSSS < 5) and progression (MSSS ≥ 5). Baseline data of subjects and plasma levels of TNF-α, sTNFR1, sTNFR2 were obtained. Results: The MS diagnosis explained 44.6% and 12.3% of TNF-α and sTNFR2 levels, respectively. Moderate/high disability and disability progression were best predicted by sTNFR1 and age (positively) and ProgMS were best predicted by sTNFR1 (positively) and sTNFR2 (negatively), coupled with age and sex. A composite score reflecting the sTNFR1/sTNFR2 ratio showed a positive association with ProgMS after adjusting for age and sex. Conclusion: Increased sTNFR1 and age were positively associated with disability and disability progression, whereas increased sTNFR1 (positively) and sTNFR2 (negatively) were associated with ProgMS, suggesting a distinct role of them in the immunopathological mechanisms of MS. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
10233830
Volume :
68
Issue :
12
Database :
Academic Search Index
Journal :
Inflammation Research
Publication Type :
Academic Journal
Accession number :
139439389
Full Text :
https://doi.org/10.1007/s00011-019-01286-0