|
Encephalomyelitis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Immunization with PLP(91-110) peptide caused atypical EAE in DRB1*0301.DQ8.IFN-γ(-/-) mice characterized by ataxia, spasticity, and dystonia, hallmarks of brain-specific disease.
|
25339670 |
2014 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
This switch defines a unique in vivo cell surface signature (CCR6(-)CCR2(+)) of GM-CSF/IFNγ-producing Th17 cells in EAE and experimental persistent extracellular bacterial infection, and in humans.
|
26511769 |
2015 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interferon gamma (IFN-γ)/tumor necrosis factor alpha (TNF-α) and interleukin-4 (IL-4)/interleukin-10 (IL-10), the hallmark cytokines that direct Th1 and Th2 development, were detected with enzyme-linked immunosorbent assay (ELISA). terminal dUTP nick-end labeling (TUNEL) staining was performed to elucidate the cell apoptosis in the spinal cords of EAE mice.
|
23826999 |
2013 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we showed that probiotic <i>Lactobacillus reuteri</i> DSM 17938 (<i>L. reuteri</i>) ameliorated the development of murine experimental autoimmune encephalomyelitis (EAE), a widely used animal model of MS, a model which is primarily mediated by T<sub>H</sub>17 and T<sub>H</sub>1 cells.We discovered that <i>L. reuteri</i> treatment reduced T<sub>H</sub>1/T<sub>H</sub>17 cells and their associated cytokines IFN-γ/IL-17 in EAE mice.
|
30899262 |
2019 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we investigated whether IFN-γ could exert a role in the anxiety- and depressive-like behavior observed in mice with EAE, and in the modulation of CB1Rs.
|
28757328 |
2017 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
APG significantly ameliorates the progression of EAE by inhibiting the proliferation of autoreactive T cells and the production of inflammatory cytokines such as IFN-γ, IL-1β and IL-17.
|
21524666 |
2011 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Specifically, MS-like lesions developed in the brain that included equal numbers of IFN-γ producing CD4(+) and CD8(+) T cells and demyelination, none of which is observed in MOG induced EAE.
|
26356194 |
2015 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, high IL-7 expression was detected in the CNS during EAE and could drive the plasticity of Th17 cells to IFN-γ-producing T cells.
|
26223651 |
2015 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
For the spinal cord, IFN-γ-deficient cells (that are ordinarily cerebellum disease initiators) were capable of driving new spinal-cord-associated clinical symptoms more than 60 days after the initial acute EAE resolution.
|
23121407 |
2013 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both CD4<sup>+</sup> and CD8<sup>+</sup> T cells were most sensitive to MOG antigen stimulation for IFN-γ production during the early stage of EAE, but then rapidly lost the function despite their vigorous proliferation at the peak stage and later.
|
28872930 |
2018 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using the experimental autoimmune encephalomyelitis model, MIS416 treatment was associated with IFN-γ-dependant expansion of Treg number and increased suppressive function; however, these cells did not account for disease reduction.
|
29321652 |
2018 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Despite normal T cell priming, <i>Sb1</i><sup>-/-</sup> mice are resistant to EAE with a paucity of T helper (T<sub>H</sub>) cells that produce two or more of the cytokines, IFNγ, GM-CSF, and IL-17.
|
31548399 |
2019 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Piwep also inhibited proliferation of lymphocytes and secretion of interferon-γ in the lymph node of EAE mice.
|
24592383 |
2014 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, the magnitudes of myelin basic protein (MBP)-induced rise in the frequency of IFN-γ+ and IL-17+ CD8+ T cells (providing important help to neuroantigen-specific CD4+ T cells in EAE models characterized by clinically mild disease) were greater in dLN cell cultures from aged AO rats.
|
29128575 |
2018 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Physical exercise inhibited the production of inflammatory cytokines, such as IFN-γ, IL-17 and IL-1β in the spinal cord after EAE induction, as well as spleen cells obtained from ST group showed a significant upregulation of regulatory T cell markers, such as CD25 and IL-10 levels, and blocked IL-6, MCP-1 and TNF-α production, mainly, during acute and chronic phase of EAE.
|
27447807 |
2017 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Treatment of EAE mice with GL from onset to the peak stage of disease resulted in marked attenuation of EAE severity, reduced inflammatory cell infiltration and demyelination, decreased tumor necrosis factor-alpha (TNF-α), IFN-γ, IL-17A, IL-6, and transforming growth factor-beta 1, and increased IL-4 both in serum and spinal cord homogenate.
|
30013568 |
2018 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Recently, Seifert and colleagues reported surprising observations concerning the functions of immunoproteasomes and cellular responses to interferon-γ: (1) that immunoproteasomes degrade ubiquitinated proteins faster than the constitutive proteasomes, (2) that polyubiquitin conjugates accumulate after interferon-γ treatment but then are preferentially degraded by immunoproteasomes, and (3) that immunoproteasome deficiency causes the formation of inclusions and more severe experimental autoimmune encephalomyelitis (EAE).
|
23452861 |
2013 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, when co-transferred with myelin-specific 2D2 TCR-transgenic naive T cells, unrelated OT-II TCR-transgenic memory-like T<sub>H</sub>17 cells infiltrate the spinal cord and produce IL-17A, interferon (IFN)-γ, and GM-CSF, increasing the susceptibility of the recipients to experimental autoimmune encephalomyelitis in an IL-1 receptor-dependent manner.
|
30755603 |
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 |
A progressive form of EAE was induced using transgenic mice expressing a dominant negative interferon-γ (IFN-γ) receptor alpha chain under control of human glial fibrillary acidic protein (GFAP) promoter (GFAPγR1Δ mice).
|
25896970 |
2015 |
|
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 |
Here, we demonstrate that B7-H3 KO mice have significantly less inflammation, decreased pathogenesis, and limited disease progression in both EAE and CIA mouse models when compared with littermates; these results were accompanied by a decrease in IFN-γ and IL-17 production.
|
26065426 |
2015 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of Myeloid Differentiation Factor 88 Reduces Human and Mouse T-Cell Interleukin-17 and IFNγ Production and Ameliorates Experimental Autoimmune Encephalomyelitis Induced in Mice.
|
28611775 |
2017 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest that, whereas IFN-γ as such is not necessary for EAE development in the mouse, the lack of suppression of Th17 cells by IFN-γ enhances the susceptibility to develop EAE.
|
21348780 |
2011 |
|
Encephalomyelitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We found that intravenous administration of exosomes produced by MSCs stimulated by IFNγ (IFNγ-Exo) (i) reduced the mean clinical score of EAE mice compared to PBS control, (ii) reduced demyelination, (iii) decreased neuroinflammation, and (iv) upregulated the number of CD4+CD25+FOXP3+ regulatory T cells (Tregs) within the spinal cords of EAE mice.
|
31117376 |
2019 |