Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Besides, proinflammatory cytokines such as, IFN-γ, TNF-α, IL-6, and IL-17 were significantly diminished in the serum and spinal cord of EAE mice receiving HIV-1 Tat clade B and C. Conversely, anti-inflammatory cytokines, including IL-10 and IL-4 were elevated in the serum and spinal cord of EAE mice receiving HIV Tat clade B and C when compared with the control group.
|
31830622 |
2020 |
Encephalomyelitis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Nox2 deletion prevented EAE-induced induction of pro-inflammatory cytokines and stimulated the expression of the anti-inflammatory cytokines IL-4 and IL-10.
|
30984416 |
2019 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Down-regulation of TUG1 improved mice behavior, reduced granulocyte-macrophage colony stimulating factor (GM-CSF) level, decreased the levels of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin (IL)-6 and IL-17, and increased IL-10 in EAE mice.
|
31394128 |
2019 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, this study evaluated the modulatory effects of Thymus vulgaris on the clinical symptoms, histopathological scores, and the production of some anti-inflammatory (TGF-β, IL-4, and IL-10) and pro-inflammatory (IFN-γ, IL-6 and IL-17) cytokines in EAE model.
|
30551467 |
2019 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We aimed to assess the Carvacrol effects on clinical manifestations and production of pro-inflammatory (IFN-γ, IL-6 and IL-17) and anti-inflammatory (TGF-β, IL-4, and IL-10) cytokines in experimental autoimmune encephalomyelitis (EAE) as MS animal model.
|
30472298 |
2019 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
THC + CBD treatment attenuated EAE and caused significant decrease in inflammatory cytokines such as IL-17 and IFN-γ while promoting the induction of anti-inflammatory cytokines such as IL-10 and TGF-β.
|
31356922 |
2019 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Random amino acid copolymers used in the treatment of multiple sclerosis in man or experimental autoimmune encephalomyelitis (EAE) in mice [poly(Y,E,A,K)<sub>n</sub>, known as Copaxone, and poly(Y,F,A,K)<sub>n</sub>] function at least in part by generation of IL-10-secreting regulatory T cells that mediate bystander immunosuppression.
|
30683721 |
2019 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study demonstrates that E2 treatment induced three heightened regulatory mechanisms that potentially protect IL-10 KO mice from EAE: (1) an increase in programmed death-ligands 1 and 2 on monocytes and macrophages in the periphery and within the CNS; (2) an increase in CD73 in the inflamed CNS, which can increase the production of the anti-inflammatory molecule adenosine; and (3) a decrease in CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup> regulatory T cells in the spleen.
|
31665042 |
2019 |
Encephalomyelitis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
However, experiments involving IL-10-deficient mice and PD-1 blockade revealed that AAV-IL-27-induced IL-10 and PD-L1 expression were not required for the prevention of EAE development.
|
29740452 |
2018 |
Encephalomyelitis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The mRNA and protein levels of interleukin-10 in the rat brain in EAE group were decreased notably (P<0.05), while those of interferon-γ and tumor necrosis factor-α were increased significantly (P<0.05).
|
30546391 |
2018 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10<sup>-/-</sup> BMDMs into mice with EAE at disease onset did not reverse disease severity, implying IL10 may be essential in lenalidomide-ameliorated EAE.
|
29445144 |
2018 |
Encephalomyelitis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In addition, adoptive transfer of CD4<sup>+</sup> T cells from GSNO treated EAE mice to active EAE mice also ameliorated EAE disease with induction of spinal cord expression of IL-10 and reduction in of IL-17, thus suggesting the participation of IL-10 mechanism in GSNO mediated immunomodulation.
|
29960806 |
2018 |
Encephalomyelitis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Multiplex cytokine assays demonstrated that mice with chronic EAE and treated with either OGF or low-dose naltrexone (LDN) had decreased expression of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and the anti-inflammatory cytokine IL-10 within 10 days or treatment, as well as increased serum expression of the pro-inflammatory cytokine IL-6, relative to immunized mice receiving saline.
|
29307283 |
2018 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The recovery of spatial memory, besides a reduction of serum leptin levels, allied to central and peripheral elevation of the anti-inflammatory cytokine IL-10, was solely modulated by CTK 01512-2, dosed intrathecally.The intravenous (i.v.) administration of CTK 01512-2 also reduced the EAE-elicited MS-like symptoms, similarly to that seen in animals that received fingolimod orally.
|
29667130 |
2018 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Fine Tuning the Cytokine Storm by IFN and IL-10 Following Neurotropic Coronavirus Encephalomyelitis.
|
30619363 |
2018 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, the shift from Th17 to Th1 responses with decreased virus virulence indicates that the effects of IL-10 deficiency on immunopathologic responses in the CNS during alphavirus infection are influenced by virus strain.<b>IMPORTANCE</b> Alphaviruses cause mosquito-borne outbreaks of encephalomyelitis, but determinants of outcome are incompletely understood.
|
29263262 |
2018 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
SR141716A significantly up-regulated the expression of toll like receptor-4 (TLR-4) and nuclear factor-kappaB/p65 (NF-κB/p65) on microglia/macrophages of EAE mice as well as levels of inflammatory factors (TNF-α, IL-1β, IL-6) and chemokines (MCP-1, CX3CL1), accompanied by the shifts of cytokines from Th2 (IL-4, IL-10) to Th1 (IFN-γ)/Th17 (IL-17) in the spinal cords of EAE mice.
|
29501084 |
2018 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Co-cultures with splenocytes isolated from EAE mice revealed transcripts of interleukin-10 and transforming growth factor-β, known promoters of regulatory T cells, that were greatly expressed in SVF cells compared to ASCs, and expression levels of signaling mediators related to effector T cells were insignificant in both SVF cells and ASCs.
|
29534751 |
2018 |
Encephalomyelitis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Of note, spleen cells obtained from strength training group incubated with MOG<sub>35-55</sub> showed a significant upregulation of CD25 and IL-10 levels, with a decrease of IL-6, MCP-1, and tumor necrosis factor (TNF)-α production, mainly, during acute and chronic phase of EAE.
|
27447807 |
2017 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Functional studies in experimental autoimmune encephalomyelitis (EAE) indicate that B-cell deficiencies, and a lack of IL10 and IL35 leads to a poor prognosis.
|
27682872 |
2017 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both IFN-β1b and IFN-β1a treatments inhibited the pro-inflammatory cytokines (IL-6, IL-1β, TNF-α and IFN-γ), decreased the activation of astrocytes, increased the myelin protein level in the brain cortex, and improved the neurological status of EAE rats by different mechanisms; IFN-β1a reduced iNOS expression, at least in part, by the enhancement of IL-10, while IFN-β1b diminished IL-10 concentration and did not decrease EAE-induced iNOS expression.
|
28299403 |
2017 |
Encephalomyelitis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Spleens from treated EAE mice revealed diminished T<sub>H</sub> 1 and T<sub>H</sub> 17 cell activities and were markedly higher in the levels of anti-inflammatory cytokine interleukin-10.
|
28801931 |
2017 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In contrast, another APL, A188, which induced IL-10 production without proliferation in CD4<sup>+</sup> T cells specific for the native encephalitogen, was able to protect against development of EAE in a dose-dependent fashion when co-immunized alongside the native encephalitogen.
|
28495132 |
2017 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we have assessed the therapeutic potential of a novel anti-inflammatory interleukin-10 (IL-10) non-viral gene therapy formulation (XT-101-R) in a rat relapsing remitting experimental autoimmune encephalomyelitis (EAE) model.
|
27189037 |
2017 |
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The aim of this study is to evaluate the overexpression of interleukin-4 (IL-4), IL-10 and leukemia inhibitory factor (LIF) in Wharton's jelly stem cells (WJSCs) in the experimental autoimmune encephalomyelitis (EAE) mice model.
|
28836399 |
2017 |