The influence of glatiramer acetate on Th17-immune response in multiple sclerosis

Autor: Svetlana N. Sharanova, Nina E. Murugina, Mikhail Pashenkov, Yulia A. Dagil, Anastasiya Sviridova, Tatiana Ospelnikova, Anna M. Nikolaeva, Vladimir V. Murugin, Vladimir Rogovskii, M V Melnikov, Alexey Boyko
Rok vydání: 2020
Předmět:
CD4-Positive T-Lymphocytes
Male
0301 basic medicine
Lipopolysaccharide
Physiology
Polymers
medicine.medical_treatment
Cancer Treatment
Pharmacology
Toxicology
Pathology and Laboratory Medicine
White Blood Cells
chemistry.chemical_compound
Medical Conditions
0302 clinical medicine
Animal Cells
Immune Physiology
Medicine and Health Sciences
Toxins
Materials
Innate Immune System
Multidisciplinary
T Cells
Chemistry
Neurodegenerative Diseases
Cell Differentiation
Cytokine
Neurology
Macromolecules
Oncology
Physical Sciences
Medicine
Cytokines
Female
Cellular Types
medicine.symptom
Immunosuppressive Agents
Research Article
medicine.drug
Adult
Multiple Sclerosis
Science
Immune Cells
Immunology
Materials Science
Toxic Agents
Bacterial Toxins
Antigen-Presenting Cells
Cytokine Therapy
Real-Time Polymerase Chain Reaction
Peripheral blood mononuclear cell
Autoimmune Diseases
Microbeads
03 medical and health sciences
Immune system
medicine
Humans
Glatiramer acetate
Blood Cells
Multiple sclerosis
Biology and Life Sciences
Cell Biology
Dendritic Cells
Glatiramer Acetate
Molecular Development
Polymer Chemistry
medicine.disease
Demyelinating Disorders
In vitro
Endotoxins
030104 developmental biology
Mechanism of action
Immune System
Leukocytes
Mononuclear
Th17 Cells
Clinical Immunology
Clinical Medicine
030217 neurology & neurosurgery
Developmental Biology
Zdroj: PLoS ONE
PLoS ONE, Vol 15, Iss 10, p e0240305 (2020)
ISSN: 1932-6203
Popis: Glatiramer acetate (GA) is approved for the treatment of multiple sclerosis (MS). However, the mechanism of action of GA in MS is still unclear. In particular, it is not known whether GA can modulate the pro-inflammatory Th17-type immune response in MS. We investigated the effects of original GA (Copaxone®, Teva, Israel) and generic GA (Timexone®, Biocad, Russia) on Th17- and Th1-type cytokine production in vitro in 25 patients with relapsing-remitting MS and 25 healthy subjects. Both original and generic GA at concentrations 50-200 μg/ml dose-dependently inhibited interleukin-17 and interferon-γ production by anti-CD3/anti-CD28-activated peripheral blood mononuclear cells from MS patients and healthy subjects. This effect of GA was reproduced using purified CD4+ T cells, suggesting that GA can directly modulate the functions of Th17 and Th1 cells. At high concentrations (100-200 μg/ml), GA also suppressed the production of Th17-differentiation cytokines (interleukin-1β and interleukin-6) by lipopolysaccharide (LPS)-activated dendritic cells (DCs). These GA/LPS-treated DCs induced lower interleukin-17 and interferon-γ production by autologous CD4+ T cells compared to LPS-treated DCs. These data suggest that GA can inhibit Th17-immune response and that this inhibitory effect is preferentially exercised by direct influence of GA on T cells. We also demonstrate a comparable ability of original and generic GA to modulate pro-inflammatory cytokine production.
Databáze: OpenAIRE
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