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experimental autoimmune encephalomyelitis

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https://www.readbyqxmd.com/read/28443093/a-novel-cervical-spinal-cord-window-preparation-allows-for-two-photon-imaging-of-t-cell-interactions-with-the-cervical-spinal-cord-microvasculature-during-experimental-autoimmune-encephalomyelitis
#1
Neda Haghayegh Jahromi, Heidi Tardent, Gaby Enzmann, Urban Deutsch, Naoto Kawakami, Stefan Bittner, Dietmar Vestweber, Frauke Zipp, Jens V Stein, Britta Engelhardt
T-cell migration across the blood-brain barrier (BBB) is a crucial step in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Two-photon intravital microscopy (2P-IVM) has been established as a powerful tool to study cell-cell interactions in inflammatory EAE lesions in living animals. In EAE, central nervous system inflammation is strongly pronounced in the spinal cord, an organ in which 2P-IVM imaging is technically very challenging and has been limited to the lumbar spinal cord...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28439012/gestational-bisphenol-a-exposure-lowers-the-threshold-for-autoimmunity-in-a-model-of-multiple-sclerosis
#2
James A Rogers, Manoj K Mishra, Jennifer Hahn, Catherine J Greene, Robin M Yates, Luanne M Metz, V Wee Yong
Environmental and hormonal factors are implicated in dysimmunity in multiple sclerosis. We investigated whether bisphenol-A, a prominent contaminant with endocrine-disrupting capabilities, altered susceptibility in an inflammatory model of multiple sclerosis. We found that gestational, but not adult, exposure to bisphenol-A increased the development of experimental autoimmune encephalomyelitis in adulthood in male, but not female, mice when a suboptimal disease-inducing immunization was used. Gestational bisphenol-A in male mice primed macrophages in adulthood and raised granulocyte-colony stimulating factor and neutrophil counts/activity postsuboptimal immunization...
April 24, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28438314/progression-of-experimental-autoimmune-encephalomyelitis-is-associated-with-up-regulation-of-major-sodium-transporters-in-the-mouse-kidney-cortex-under-a-normal-salt-diet
#3
Xiaoming Zhou, Balamurugan Packialakshmi, Yao Xiao, Saule Nurmukhambetova, Jason R Lees
Recent demonstrations of exacerbation of experimental autoimmune encephalomyelitis (EAE) by high salt diets prompted us to study whether EAE stimulated Na absorption by the renal cortex, a primary regulatory site for Na balance, even under a normal NaCl diet. We found that as EAE progressed from mild to severe symptoms, there were parallel increases in the protein abundance of NHE3 and αENaC and the Na,K-ATPase activity with an affiliated elevation of its β1-subunit protein. These effects are associated with increases in the protein levels of the well-known regulators SGK1 and scaffold NHERF2, and phosphorylation of ERK1/2...
April 18, 2017: Cellular Immunology
https://www.readbyqxmd.com/read/28436428/neuronal-ifn-beta-induced-pi3k-akt-foxa1-signalling-is-essential-for-generation-of-foxa1-treg-cells
#4
Yawei Liu, Andrea Marin, Patrick Ejlerskov, Louise Munk Rasmussen, Marco Prinz, Shohreh Issazadeh-Navikas
Neurons reprogramme encephalitogenic T cells (Tenc) to regulatory T cells (Tregs), either FoxP3(+)Tregs or FoxA1(+)Tregs. We reported previously that neuronal ability to generate FoxA1(+)Tregs was central to preventing neuroinflammation in experimental autoimmune encephalomyelitis (EAE). Mice lacking interferon (IFN)-β were defective in generating FoxA1(+)Tregs in the brain. Here we show that lack of neuronal IFNβ signalling is associated with the absence of programme death ligand-1 (PDL1), which prevents their ability to reprogramme Tenc cells to FoxA1(+)Tregs...
April 24, 2017: Nature Communications
https://www.readbyqxmd.com/read/28435673/primate-autoimmune-disease-models-lost-for-translation
#5
Bert A 't Hart
Replacement, reduction and refinement (the 3R's) are the leading principles in translational research with animals. To be useful a model should also be clinically Relevant (the 4th R). Work in a non-human primate model of multiple sclerosis, the experimental autoimmune encephalomyelitis model, reveals an inherent conflict among these 4R principles. The impossibility to harmonize all 4R's forms a major challenge when the model is applied in preclinical drug development.
December 2016: Clinical & Translational Immunology
https://www.readbyqxmd.com/read/28431621/two-decades-of-glatiramer-acetate-from-initial-discovery-to-the-current-development-of-generics
#6
REVIEW
Bianca Weinstock-Guttman, Kavita V Nair, Joseph L Glajch, Tanmoy C Ganguly, Daniel Kantor
Multiple sclerosis (MS) is a chronic, incurable, inflammatory disease of the central nervous system (CNS). In the United States, several US Food and Drug Administration (FDA)-approved disease-modifying treatments (DMTs) are available, including glatiramer acetate (GA; Copaxone®), one of the most longstanding treatments. GA was discovered serendipitously in the late 1960s/early 1970s while attempting to produce a synthetic antigen capable of inducing experimental autoimmune encephalomyelitis (EAE), an animal model of autoimmune inflammatory CNS disorders, including MS...
May 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28426455/digoxin-attenuates-murine-experimental-colitis-by-downregulating-th17-related-cytokines
#7
Shinya Tani, Ryosuke Takano, Satoshi Tamura, Shinji Oishi, Moriya Iwaizumi, Yasushi Hamaya, Kosuke Takagaki, Toshi Nagata, Shintaro Seto, Toshinobu Horii, Isao Kosugi, Toshihide Iwashita, Satoshi Osawa, Takahisa Furuta, Hiroaki Miyajima, Ken Sugimoto
BACKGROUND: Digoxin, a cardiac glycoside used for the treatment of heart failure, was reported to inhibit the retinoid-related orphan receptor gamma t (RORγt) and attenuate the severity of experimental autoimmune encephalomyelitis and arthritis in mice. However, the effects of digoxin in a mice model of inflammatory bowel disease have not been elucidated. METHODS: Colitis was induced in severe combined immunodeficiency mice by adoptive transfer of CD45RB CD4 T cells...
May 2017: Inflammatory Bowel Diseases
https://www.readbyqxmd.com/read/28425447/development-and-pre-clinical-evaluation-of-recombinant-human-myelin-basic-protein-nano-therapeutic-vaccine-in-experimental-autoimmune-encephalomyelitis-mice-animal-model
#8
Medhat A Al-Ghobashy, Aliaa N ElMeshad, Rania M Abdelsalam, Mohammed M Nooh, Muhammad Al-Shorbagy, Götz Laible
Recombinant human myelin basic protein (rhMBP) was previously produced in the milk of transgenic cows. Differences in molecular recognition of either hMBP or rhMBP by surface-immobilized anti-hMBP antibodies were demonstrated. This indicated differences in immunological response between rhMBP and hMBP. Here, the activity of free and controlled release rhMBP poly(ε-caprolactone) nanoparticles (NPs), as a therapeutic vaccine against multiple sclerosis (MS) was demonstrated in experimental autoimmune encephalomyelitis (EAE) animal model...
April 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28425078/involvement-of-interstitial-cells-of-cajal-in-bladder-dysfunction-in-mice-with-experimental-autoimmune-encephalomyelitis
#9
Zhibo Jin, Yinghui Ding, Rui Xue, Zhankui Jia, Zhenlin Huang, Yafei Ding, Chaohui Gu, Jinjian Yang
BACKGROUND: Bladder dysfunction is an important symptom of experimental autoimmune encephalomyelitis (EAE). Our previous study showed that EAE-induced upregulation of the E-prostanoid receptor 3 (EP3) and E-prostanoid receptor 4 (EP4) in the bladder was accompanied by bladder dysfunction. Although many other studies have evaluated the lower urinary tract symptoms in multiple sclerosis, the mechanism remains unclear. OBJECTIVES: To investigate the effects of interstitial cells of Cajal (ICC) on bladder dysfunction in a novel neurogenic bladder model induced by experimental autoimmune encephalomyelitis...
April 19, 2017: International Urology and Nephrology
https://www.readbyqxmd.com/read/28424240/the-histone-acetyltransferase-gcn5-positively-regulates-t-cell-activation
#10
Beixue Gao, Qingfei Kong, Yana Zhang, Chawon Yun, Sharon Y R Dent, Jianxun Song, Donna D Zhang, Yiming Wang, Xuemei Li, Deyu Fang
Histone acetyltransferases (HATs) regulate inducible transcription in multiple cellular processes and during inflammatory and immune response. However, the functions of general control nonrepressed-protein 5 (Gcn5), an evolutionarily conserved HAT from yeast to human, in immune regulation remain unappreciated. In this study, we conditionally deleted Gcn5 (encoded by the Kat2a gene) specifically in T lymphocytes by crossing floxed Gcn5 and Lck-Cre mice, and demonstrated that Gcn5 plays important roles in multiple stages of T cell functions including development, clonal expansion, and differentiation...
April 19, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28421297/suppression-of-th1-differentiation-by-tryptophan-supplementation-in-vivo
#11
Tobias V Lanz, Simon Becker, Soumya R Mohapatra, Christiane A Opitz, Wolfgang Wick, Michael Platten
Metabolism of the essential amino acid tryptophan (trp) is a key endogenous immunosuppressive pathway restricting inflammatory responses. Tryptophan metabolites promote regulatory T cell (Treg) differentiation and suppress proinflammatory T helper cell (Th)1 and Th17 phenotypes. It has been shown that treatment with natural and synthetic tryptophan metabolites can suppress autoimmune neuroinflammation in preclinical animal models. Here, we tested if oral intake of tryptophan would increase immunosuppressive tryptophan metabolites and ameliorate autoimmune neuroinflammation as a safe approach to treat autoimmune disorders like multiple sclerosis (MS)...
April 18, 2017: Amino Acids
https://www.readbyqxmd.com/read/28421248/indications-for-cellular-migration-from-the-central-nervous-system-to-its-draining-lymph-nodes-in-cd11c-gfp-bone-marrow-chimeras-following-eae
#12
Fridtjof Schiefenhövel, Kerstin Immig, Carolin Prodinger, Ingo Bechmann
The concept as to how the brain maintains its immune privilege has initially been based on observations that it is lacking classical lymph vessels and later, the absence of dendritic cells (DC). This view has been challenged by several groups demonstrating drainage/migration of injected tracers and cells into cervical lymph nodes (CLNs) and the presence of brain antigens in CLNs in the course of various brain pathologies. Using CD11c-diphtheria toxin receptor (DTR)-green fluorescent protein (GFP) transgenic (tg) mice, we have shown the existence of CD11c(+) cells, a main DC marker, within the brain parenchyma...
April 18, 2017: Experimental Brain Research. Experimentelle Hirnforschung. Expérimentation Cérébrale
https://www.readbyqxmd.com/read/28417055/potential-involvement-of-glycogen-synthase-kinase-gsk-3%C3%AE-in-a-rat-model-of-multiple-sclerosis-evidenced-by-lithium-treatment
#13
Meejung Ahn, Jeongtae Kim, Changnam Park, Jinhee Cho, Youngheun Jee, Kyungsook Jung, Changjong Moon, Taekyun Shin
Glycogen synthase kinase (GSK)-3β has been known as a pro-inflammatory molecule in neuroinflammation. The involvement of GSK-3β remains unsolved in acute monophasic rat experimental autoimmune encephalomyelitis (EAE). The aim of this study was to evaluate a potential role of GSK-3β in central nervous system (CNS) autoimmunity through its inhibition by lithium. Lithium treatment significantly delayed the onset of EAE paralysis and ameliorated its severity. Lithium treatment reduced the serum level of pro-inflammatory tumor necrosis factor a but not that of interleukin 10...
March 2017: Anatomy & Cell Biology
https://www.readbyqxmd.com/read/28416719/correction-cutting-edge-integrin-%C3%AE-4-is-required-for-regulatory-b-cell-control-of-experimental-autoimmune-encephalomyelitis
#14
Simon Glatigny, Catriona A Wagner, Estelle Bettelli
No abstract text is available yet for this article.
May 1, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28416715/t-cell-transfer-experimental-autoimmune-encephalomyelitis-pillar-of-multiple-sclerosis-and-autoimmunity
#15
Reinhard Hohlfeld, Lawrence Steinman
No abstract text is available yet for this article.
May 1, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28411187/the-nuclear-receptor-nr4a1-acts-as-a-microglia-rheostat-and-serves-as-a-therapeutic-target-in-autoimmune-driven-central-nervous-system-inflammation
#16
Tobias Rothe, Natacha Ipseiz, Maria Faas, Stefanie Lang, Francesc Perez-Branguli, Daniel Metzger, Hiroshi Ichinose, Beate Winner, Georg Schett, Gerhard Krönke
Microglia cells fulfill key homeostatic functions and essentially contribute to host defense within the CNS. Altered activation of microglia, in turn, has been implicated in neuroinflammatory and neurodegenerative diseases. In this study, we identify the nuclear receptor (NR) Nr4a1 as key rheostat controlling the activation threshold and polarization of microglia. In steady-state microglia, ubiquitous neuronal-derived stress signals such as ATP induced expression of this NR, which contributed to the maintenance of a resting and noninflammatory microglia phenotype...
April 14, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28405624/gm-csf-is-not-essential-for-experimental-autoimmune-encephalomyelitis-but-promotes-brain-targeted-disease
#17
Emily R Pierson, Joan M Goverman
Experimental autoimmune encephalomyelitis (EAE) has been used as an animal model of multiple sclerosis to identify pathogenic cytokines that could be therapeutic targets. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is the only cytokine reported to be essential for EAE. We investigated the role of GM-CSF in EAE in C3HeB/FeJ mice that uniquely exhibit extensive brain and spinal cord inflammation. Unexpectedly, GM-CSF-deficient C3HeB/FeJ mice were fully susceptible to EAE because IL-17 activity compensated for the loss of GM-CSF during induction of spinal cord-targeted disease...
April 6, 2017: JCI Insight
https://www.readbyqxmd.com/read/28400721/mir-384-regulates-the-th17-treg-ratio-during-experimental-autoimmune-encephalomyelitis-pathogenesis
#18
Xuebin Qu, Jingjing Han, Ying Zhang, Yuanyuan Wang, Jun Zhou, Hongbin Fan, Ruiqin Yao
Specific miRNAs are involved in the pathogenesis of multiple sclerosis (MS), during which IL-17-producing CD4(+) T helper (Th17) cells accumulate in the central nervous system (CNS). In this study, we identified levels of miR-384 as significantly increased in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Over-expression of miR-384 in vivo led to severe EAE, characterized by exacerbated demyelination, and increased inflammatory cell infiltration of the spinal cord; inhibition of miR-384 reversed these changes...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28400474/suppression-of-th17-cell-differentiation-by-misshapen-nik-related-kinase-mink1
#19
Guotong Fu, Qin Xu, Yuanjun Qiu, Xuexiao Jin, Ting Xu, Shunli Dong, Jianli Wang, Yuehai Ke, Hu Hu, Xuetao Cao, Di Wang, Harvey Cantor, Xiang Gao, Linrong Lu
T helper type 17 cells (Th17 cells) are major contributors to many autoimmune diseases. In this study, we demonstrate that the germinal center kinase family member MINK1 (misshapen/NIK-related kinase 1) negatively regulates Th17 cell differentiation. The suppressive effect of MINK1 on induction of Th17 cells is mediated by the inhibition of SMAD2 activation through direct phosphorylation of SMAD2 at the T324 residue. The importance of MINK1 to Th17 cell differentiation was strengthened in the animal model of experimental autoimmune encephalomyelitis (EAE)...
April 11, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28397727/neutralization-of-interleukin-9-decreasing-mast-cells-infiltration-in-experimental-autoimmune-encephalomyelitis
#20
Jun-Jie Yin, Xue-Qiang Hu, Zhi-Feng Mao, Jian Bao, Wei Qiu, Zheng-Qi Lu, Hao-Tian Wu, Xiao-Nan Zhong
BACKGROUND: Th9 cells are a newly discovered CD4+ T helper cell subtype, characterized by high interleukin (IL)-9 secretion. Growing evidences suggest that Th9 cells are involved in the pathogenic mechanism of multiple sclerosis (MS). Mast cells are multifunctional innate immune cells, which are perhaps best known for their role as dominant effector cells in allergies and asthma. Several lines of evidence point to an important role for mast cells in MS and its animal models. Simultaneously, there is dynamic "cross-talk" between Th9 and mast cells...
April 20, 2017: Chinese Medical Journal
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