Blood samples from untreated patients diagnosed with clinically isolated syndrome (CIS) (<i>n</i> = 21), different clinical forms of MS (<i>n</i> = 62) [relapsing-remitting (RRMS), secondary progressive, and primary progressive], and healthy controls (HCs) (<i>n</i> = 17) were tested for plasma levels of interferon (IFN)-γ, IL-10, TGF-β, IL-17A, and IL-17F by immunoanalysis.
The aim of this study was to investigate the vitamin D effects on the expression level of IL-6 and IL-17A in peripheral blood mononuclear cells (PBMCs) of multiple sclerosis (MS) patients.
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.
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.
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.
T-helper 17 (Th17) cells, a recently identified CD4+ T subset with a unique characteristic to produce Interleukin-17 (IL-17), are critical for the development of autoimmune diseases such as multiple sclerosis, in which IL-23 plays an important role in the differentiation of Th17 cells through IL-23/IL-23-receptor/STAT3 pathway.
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.
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.
Our objective was to find a connection between serum levels of interleukin (IL)-10, IL-17 and transforming growth factor beta (TGF-β)1 in MS patients treated with IFN-β in order to identify the nonresponders (NR).
The interleukin (IL) -23/IL-17 cytokine axis has been suggested to play an important role in the development of several autoimmune diseases including multiple sclerosis.
Interleukin 17 (IL-17) is increasingly recognized as a key factor that contributes to the pathogenesis of multiple sclerosis (MS) and its experimental mouse autoimmune encephalomyelitis (EAE) model.
Such interactions between IL-17A and glutamate excitotoxicity implicate the potential link between inflammation and neurodegeneration during MS pathogenesis, and identify astrocytes as a potential target in achieving neuroprotective effects in MS.
In this study, T-cell proliferation and IL-17 production were less sensitive to hydrocortisone (HC) inhibition in MS patients than healthy individuals, mainly in CD8(+) compartment.
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.
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.
Together, these data implicate a critical role of CaMKIIα as a cellular mechanism for pain and neuropathy in multiple sclerosis and IL-17 may act upstream of CaMKIIα in the generation of pain.<b>SIGNIFICANCE STATEMENT</b> Pain is highly prevalent in patients with multiple sclerosis (MS), significantly reducing patients' quality of life.