scholarly journals Induction of experimental autoimmune encephalomyelitis in transgenic mice expressing ovalbumin in oligodendrocytes

2006 ◽  
Vol 36 (1) ◽  
pp. 207-215 ◽  
Author(s):  
Yi Cao ◽  
Catherine Toben ◽  
Shin-Young Na ◽  
Kirsten Stark ◽  
Lars Nitschke ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals Motor neuron pathology in experimental autoimmune encephalomyelitis: studies in THY1-YFP transgenic mice

Brain ◽  
2005 ◽  
Vol 128 (8) ◽  
pp. 1877-1886 ◽  
Author(s):  
P. G. Bannerman ◽  
A. Hahn ◽  
S. Ramirez ◽  
M. Morley ◽  
C. Bönnemann ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Motor Neuron ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals Human Commensal Prevotella histicola Ameliorates Disease as Effectively as Interferon-Beta in the Experimental Autoimmune Encephalomyelitis

2020 ◽  
Vol 11 ◽  
Author(s):  
Shailesh K. Shahi ◽  
Samantha N. Jensen ◽  
Alexandra C. Murra ◽  
Na Tang ◽  
Hui Guo ◽  
...  
Keyword(s):  
T Cells ◽  
Environmental Factors ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Gut Microbiota ◽  
Transgenic Mice ◽  
Environmental Factor ◽  
Interferon Beta ◽  
Hla Class Ii ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Gut microbiota has emerged as an important environmental factor in the pathobiology of multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS). Both genetic and environmental factors have been shown to play an important role in MS. Among genetic factors, the human leukocyte antigen (HLA) class II allele such as HLA-DR2, DR3, DR4, DQ6, and DQ8 show the association with the MS. We have previously used transgenic mice expressing MS susceptible HLA class II allele such as HLA-DR2, DR3, DQ6, and DQ8 to validate significance of HLA alleles in MS. Although environmental factors contribute to 2/3 of MS risk, less is known about them. Gut microbiota is emerging as an imporatnt environmental factor in MS pathogenesis. We and others have shown that MS patients have distinct gut microbiota compared to healthy control (HC) with a lower abundance of Prevotella. Additionally, the abundance of Prevotella increased in patients receiving disease-modifying therapies (DMTs) such as Copaxone and/or Interferon-beta (IFNβ). We have previously identified a specific strain of Prevotella (Prevotella histicola), which can suppress experimental autoimmune encephalomyelitis (EAE) disease in HLA-DR3.DQ8 transgenic mice. Since Interferon-β-1b [IFNβ (Betaseron)] is a major DMTs used in MS patients, we hypothesized that treatment with the combination of P. histicola and IFNβ would have an additive effect on the disease suppression. We observed that treatment with P. histicola suppressed disease as effectively as IFNβ. Surprisingly, the combination of P. histicola and IFNβ was not more effective than either treatment alone. P. histicola alone or in combination with IFNβ increased the frequency and number of CD4+FoxP3+ regulatory T cells in the gut-associated lymphoid tissue (GALT). Treatment with P. histicola alone, IFNβ alone, and in the combination decreased frequency of pro-inflammatory IFN-γ and IL17-producing CD4+ T cells in the CNS. Additionally, P. histicola alone or IFNβ alone or the combination treatments decreased CNS pathology, characterized by reduced microglia and astrocytic activation. In conclusion, our study indicates that the human gut commensal P. histicola can suppress disease as effectively as commonly used MS drug IFNβ and may provide an alternative treatment option for MS patients.

Complementation between specific HLA-DR and HLA-DQ genes in transgenic mice determines susceptibility to experimental autoimmune encephalomyelitis

2000 ◽  
Vol 61 (3) ◽  
pp. 279-289 ◽  
Author(s):  
Pritam Das ◽  
Kristen M Drescher ◽  
Annemieke Geluk ◽  
David S Bradley ◽  
Moses Rodriguez ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Autoimmune Encephalomyelitis ◽  
Hla Dr ◽  
Hla Dq ◽  
Experimental Autoimmune

scholarly journals Inhibition of Experimental Autoimmune Encephalomyelitis in Human C-Reactive Protein Transgenic Mice Is FcRIIB Dependent

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Xian-Zhen Hu ◽  
Tyler T. Wright ◽  
Nicholas R. Jones ◽  
Theresa N. Ramos ◽  
Gregory A. Skibinski ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Fc Receptors ◽  
Subcutaneous Administration ◽  
Wild Type ◽  
C Reactive Protein ◽  
Autoimmune Encephalomyelitis ◽  
Similar Treatment ◽  
Reactive Protein ◽  
Experimental Autoimmune

We showed earlier that experimental autoimmune encephalomyelitis (EAE) in human C-reactive protein (CRP) transgenic mice (CRPtg) has delayed onset and reduced severity compared to wild-type mice. Since human CRP is known to engage Fc receptors and Fc receptors are known to play a role in EAE in the mouse, we sought to determine if FcRI, FcRIIb, or FcRIII was needed to manifest human CRP-mediated protection of CRPtg. We report here that in CRPtg lacking either of the two activating receptors, FcRI and FcRIII, the beneficial effects of human CRP are still observed. In contrast, if CRPtg lack expression of the inhibitory receptor FcRIIB, then the beneficial effect of human CRP is abrogated. Also, subcutaneous administration of purified human CRP stalled progression of ongoing EAE in wild-type mice, but similar treatment failed to impede EAE progression in mice lacking FcRIIB. The results reveal that a axis is responsible for protection against EAE in the CRPtg model.

scholarly journals Hepatic but Not CNS-Expressed Human C-Reactive Protein Inhibits Experimental Autoimmune Encephalomyelitis in Transgenic Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Tyler T Wright ◽  
Rachel V. Jimenez ◽  
Todd E. Morgan ◽  
Namrata Bali ◽  
Xiaogang Hou ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Gene Promoter ◽  
C Reactive Protein ◽  
Autoimmune Encephalomyelitis ◽  
Reactive Protein ◽  
Protective Actions ◽  
Dependent Protein ◽  
Low Levels ◽  
Experimental Autoimmune

We recently demonstrated that human C-reactive protein (CRP), expressed hepatically in transgenic mice (CRPtg), improved the outcome of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). The liver is the primary site of CRP synthesis in humans and in CRPtg mice but is also expressed by both at low levels in the CNS. To determine if CNS expression of human CRP is sufficient to impact EAE, we generated neuronal CRP transgenic mice (nCRPtg) wherein human CRP expression is driven by the neuron-specific Ca2+/calmodulin-dependent protein kinase IIα(CaMKIIα) gene promoter. We found that hepatically expressed/blood-borne CRP, but not CNS expressed CRP, lessened EAE severity. These outcomes indicate that the protective actions of human CRP in EAE are manifested in the periphery and not in the CNS and reveal a previously unappreciated site specificity for the beneficial actions of CRP in CNS disease.

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