Alterations in serum levels of IL-17 in contrast to TNF-alpha correspond to disease-modifying treatment in relapsing-remitting multiple sclerosis.
Cytokines of different types play an important role in multiple sclerosis (MS) pathogenesis as mediators and regulators of the immune processes in the central nervous system. The aim of the study was to determine the effect of interferon-beta and glatiramer acetate on serum concentrations of TNF-alpha and IL-17 A and their correlation with the degree of disability in clinically stable patients with relapsing-remitting MS. A cross-sectional, case-control study of 220 patients (68 treatment naïve; 152 treated with interferon-beta or glatiramer acetate) and 99 clinically healthy age-gender-body mass index-matched subjects were performed. Serum cytokine concentrations were measured during remission of the disease by means of ELISA. Treatment naïve patients showed significantly higher levels of IL-17 A than the treated individuals (p = .000109) and controls (p = .000044). Within the treated group, only patients with interferon-beta had significantly higher serum IL-17 than the controls (p = .023). TNF-alpha concentrations were significantly higher in the treated patients compared to the healthy controls (p = .000013), regardless of the type of the therapy. Treatment naïve individuals did not differ from the controls according to their serum TNF-alpha (p = .922). No correlation was found between the serum cytokine concentrations and Expanded Disability Status Scale (EDSS) score (p > .05). Serum concentrations of these cytokines could not be regarded as reliable predictors for the severity of the residual neurological deficit during disease-modifying treatment. Our data suggest that suppression of IL-17 A production as one of the mechanisms underlying the beneficial effect of first-line disease-modifying treatments is stronger in glatiramer acetate than in interferon-beta.
a Department of Neurology , Medical University of Plovdiv , Plovdiv , Bulgaria.
Anastasiya Georgieva
AG
Trenova
a Department of Neurology , Medical University of Plovdiv , Plovdiv , Bulgaria.
Georgi Svetoslavov
GS
Slavov
a Department of Neurology , Medical University of Plovdiv , Plovdiv , Bulgaria.
Maria Georgieva
MG
Manova
b Department of Medical Biology , Medical University of Plovdiv , Plovdiv , Bulgaria.
Milena Nenkova
MN
Draganaova-Filipova
c Department of Medical Informatics, Biostatistics and Electronic Education, Medical Faculty , Medical University of Plovdiv , Plovdiv , Bulgaria.
Nonka Georgieva
NG
Mateva
d Department of Molecular Biology, Immunology and Medical Genetics, Medical Faculty , Trakia University , Stara Zagora , Bulgaria.
Lyuba Dineva
LD
Miteva
d Department of Molecular Biology, Immunology and Medical Genetics, Medical Faculty , Trakia University , Stara Zagora , Bulgaria.
Spaska Angelova
SA
Stanilova
D000328:Adult; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D000068717:Glatiramer Acetate / Q000627:therapeutic use; D006801:Humans; D016899:Interferon-beta / Q000627:therapeutic use; D020381:Interleukin-17 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
D020381:Interleukin-17; D014409:Tumor Necrosis Factor-alpha; D000068717:Glatiramer Acetate; D016899:Interferon-beta
Cytokines; IL-17A; disease-modifying therapy; glatiramer acetate; interferon-beta; multiple sclerosis