Prediction of disease severity in neuromyelitis optica by the levels of interleukin (IL)-6 produced during remission phase
Autor: | Priscila O. Barros, Joana Hygino, Romain Marignier, Cleonice A.M. Bento, Newton Centurião, Regina Maria Papais Alvarenga, Ulisses C. Linhares, Tatiane Cassano, Regis M. Andrade, Thais B. Ferreira, Taissa M. Kasahara, Arnaldo F.B. Andrade, Claudia Cristina Ferreira Vasconcelos |
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Rok vydání: | 2015 |
Předmět: |
Adult
CD4-Positive T-Lymphocytes Male 0301 basic medicine Hydrocortisone T cell Immunology Drug Resistance Antibodies Monoclonal Humanized Severity of Illness Index 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Tocilizumab medicine Humans Immunology and Allergy Neuromyelitis optica biology Interleukin-6 business.industry Interleukins Interleukin-17 Neuromyelitis Optica Remission Induction Autologous Monocytes Interleukin Original Articles Middle Aged medicine.disease Receptors Interleukin-6 Interleukin-10 Interleukin 10 030104 developmental biology medicine.anatomical_structure chemistry Leukocytes Mononuclear biology.protein Th17 Cells Female Interleukin 17 Antibody business 030217 neurology & neurosurgery Follow-Up Studies |
Zdroj: | Clinical and Experimental Immunology. 183:480-489 |
ISSN: | 1365-2249 0009-9104 |
Popis: | Summary T helper type 17 (Th17) cytokines have been implicated in the pathogenesis of neuromyelitis optica (NMO). As humanized anti-interleukin (IL)-6R (tocilizumab) immunoglobulin (Ig)G has been used as disease-modifying therapy for NMO, the objective of our study was to investigate the role of endogenous IL-6 on NMO-derived CD4+ T cell behaviour. High production of IL-6, IL-17 and IL-21 by CD4+ T-cells was detected in NMO patients. Further, IL-21 and IL-6 levels were related directly to the level of neurological disabilities. The addition of anti-IL-6R IgG not only reduced directly the production of these cytokines, but also almost abolished the ability of activated autologous monocytes in enhancing IL-6, IL-17 and IL-21 release by CD4+ T cells. In contrast, the production of IL-10 was amplified in those cell cultures. Further, anti-IL-6R monoclonal antibodies (mAb) also potentiated the ability of glucocorticoid in reducing Th17 cytokines. Finally, the in-vivo and in-vitro IL-6 levels were significantly higher among those patients who experienced clinical relapse during 2-year follow-up. In summary, our results suggest a deleterious role of IL-6 in NMO by favouring, at least in part, the expansion of corticoid-resistant Th17 cells. |
Databáze: | OpenAIRE |
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