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Clin Exp Immunol ; 183(3): 480-9, 2016 Mar.
Article in English | MEDLINE | ID: mdl-26472479

ABSTRACT

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.


Subject(s)
Interleukin-6/physiology , Neuromyelitis Optica/drug therapy , Neuromyelitis Optica/immunology , Adult , Antibodies, Monoclonal, Humanized/pharmacology , Antibodies, Monoclonal, Humanized/therapeutic use , CD4-Positive T-Lymphocytes , Drug Resistance , Female , Follow-Up Studies , Humans , Hydrocortisone/pharmacology , Interleukin-10/blood , Interleukin-17/blood , Interleukins/biosynthesis , Leukocytes, Mononuclear/drug effects , Male , Middle Aged , Receptors, Interleukin-6/metabolism , Remission Induction , Severity of Illness Index , Th17 Cells/drug effects , Th17 Cells/immunology
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