Mitigated Tregs and Augmented Th17 Cells and Cytokines are Associated with Severity of Experimental Autoimmune Neuritis. (September 2014)

• Record Type: Journal Article
• Authors: Wang, X.; Zheng, X.‐Y.; Ma, C.; Wang, X.‐K.; Wu, J.; Adem, A.; Zhu, J.; Zhang, H.‐L.
• Is Part Of: Scandinavian journal of immunology. Volume 80:Number 3(2014:Sep.)
• Page Start: 180
• Page End: 190
• Publication Date: 2014-09
• Subjects: Immunology -- Periodicals; 571.96
• DOI: 10.1111/sji.12201
• Languages: English
• ISSNs: 0300-9475

Abstract

<abstract abstract-type="main" id="sji12201-abs-0001"> <title>Abstract</title> <p>Experimental autoimmune neuritis (EAN), an animal model of human Guillain–Barré syndrome, has long been considered as a T helper (Th) 1 cell–mediated autoimmune disorder. However, deficiency of IFN‐<italic>γ</italic>, a signature Th1 cytokine, aggravated EAN, with features of elevated production of IL‐17A, despite an alleviated systemic Th1 immune response. We hypothesized that Th17 cells and their cytokines might play a pathogenic role in EAN. To further clarify the roles of these Th and regulatory T cell (Treg) cytokines in the pathogenesis of EAN and their interrelationship, we investigated the expression of Th1/Th2/Th17/Treg cytokines in EAN in this study. We found that the levels of Th17 cells and IL‐17A in cauda equina (CE)‐infiltrating cells and splenic mononuclear cells (MNCs) as well as in serum paralleled the disease evolution, which increased progressively during the initiation stage and reached higher value at the peak of EAN. The same pattern was also noticed for the expression of IL‐22. The diverse expression profiles of FoxP3, IL‐17 receptors A and C were seen in CE‐infiltrating cells and splenic MNCs in EAN. These findings indicate a major pro‐inflammatory role of Th17 cells and IL‐17A in the pathogenesis of EAN. Therapeutic interventions may be focused upon inhibiting Th17 cells and their cytokines in the early phase of EAN, so as to delay and suppress clinical signs of the disease, which has relevance for future studies on pathogenesis and treatment of GBS in humans.</p> </abstract>