Our work consists of a pilot study to characterize circulating Th/c1, Th/c2, Th/c17, Treg and Tfh-like populations and IL-17 serum levels of relapsing-remitting (RR) MS patients treated with IFN-β, compared with healthy controls.
The signaling elicited by the cytokine interleukin-17A (IL-17) is important for antimicrobial defense responses, whereas excessive IL-17 production leads to autoimmune diseases such as psoriasis and multiple sclerosis.
Since the main cause of MS remains obscure, in this study, we aimed to evaluate the serum levels of some cytokines, including interleukin-5 (IL-5), IL-8, IL-9, IL-17A, transforming growth factor-beta (TGF-β), and interferon-gamma (IFN-γ) in relapsing-remitting (RR)-MS patients, treated with IFN-β and glatiramer acetate (GA).
IL-17-producing T<sub>H</sub>17 cells have been associated with autoimmune diseases such as multiple sclerosis (MS), psoriasis, Crohn's disease, and ulcerative colitis (Han et al., 2015), many of which lack effective therapies.
In this study, the effects of curcumin has been investigated on the expression levels of selected cytokine coding genes as well as the extent of demyelination in the corpus callosum of C57BL/6 experimental autoimmune encephalomyelitis (EAE) model of MS. Gene expression analyses revealed that treatment with curcumin could lead to a significant reduction in the expression levels of pro-inflammatory cytokine coding genes including IL-6 (p = 0.001), IL-17 (p = 0.001), tumor necrosis factor (TNF)-α (p = 0.008), and interferon (IFN)-γ (p = 0.033) as well as a significant increase in the expression level of transforming growth factor (TGF)-β (p = 0.006) as an anti-inflammatory cytokine.
Moreover, we illustrated that proinflammatory cytokine levels include IFN-γ, TNF-α, IL-6, and IL-17 in MS patients infected with HP were lower than seronegative MS patients.
The course of MS is associated with the secretion of many inflammatory and oxidative stress mediators, including cytokines (IL-1b, IL-6, IL-17, TNF-α, INF-γ) and chemokines (MIP-1a, MCP-1, IP10).
<b>Conclusion:</b> Our findings reveal a novel pathway from the presentation of Mye-GalCer to IL-17 production, and highlight the promising therapeutic potential of D-sphingosine for the human disorder of multiple sclerosis.
IL-17-producing CD8<sup>+</sup> (Tc17) cells are enriched in active lesions of patients with multiple sclerosis (MS), suggesting a role in the pathogenesis of autoimmunity.
Consequently, blocking IL-17 has become an effective strategy for modulating several autoimmune diseases, including multiple sclerosis (MS), psoriasis, and rheumatoid arthritis (RA).
The changes in pro-inflammatory cytokine levels (IL-1β, TNF-α, IFN- γ, IL-2, IL-6, and IL-17) in the serum and supernatant of MS patients were not significant (p > 0.05).
A higher number of IFNγ (P = 0.001), IL-22 (P = 0.003), IL-17A (P < 0.0001) as well as double and triple cytokine producing MOG-specific T-cells were detected in persons with MS compared to HCs.
Pharmacological blockade of α<sub>1</sub>-adrenoceptor is shown to influence development of experimental autoimmune encephalomyelitis (EAE), an IL-17-producing CD4+TCR+ (Th17) cell-mediated disease mimicking multiple sclerosis.
In this study, we found that miR-23b, in addition to its reported functions in the suppression of IL-17-associated autoimmune inflammation, halted the progression of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by directly inhibiting the migration of pathogenic leukocytes to the CNS.
Proinflammatory cytokines such as interleukin-17 (IL-17), IL-22, tumor necrosis factor-α, IL-1, IL-12 and interferon-γ may cause MS through several signaling pathways.
Research on T cell subsets involved in MS pathogenesis has mainly focused on classical CD4<sup>+</sup> T cells, especially Th17 cells, as they produce the proinflammatory, MS-associated cytokine IL-17.
Th17 cells are a class of Th cells that secrete IL-17 and mediate pathogenic immunity responsible for autoimmunity including experimental autoimmune encephalomyelitis, a murine model of multiple sclerosis.