Animal Models of Multiple Sclerosis

Young, Colin R.; Welsh, C. Jane

doi:10.1007/978-1-59745-285-4_69

Cited by 3 publications

(9 citation statements)

References 72 publications

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“…In contrast, infection with tissue-culture-passaged DA does not result in acute disease, but the late persistent demyelinating infection of the white matter with gait disturbance is still apparent [ 24 ]. Viral persistence is necessary for the induction of the demyelinating disease [ 145 , 146 ].…”

Section: The Diseasementioning

confidence: 99%

“…Experimentation and tissue culture adaptation of the three viruses discussed in this review have led to well-characterized models using defined viral strains and titers and defined routes of infection in susceptible mouse strains of defined gender and age, as the ability of various viruses to cause disease and demyelination in mice often depends on such variables. All three viral infections give rise to inflammatory demyelinating lesions of the CNS (brain and/or spinal cord), but not in the peripheral nervous system, reflective of what is seen with MS [ 146 ].…”

Section: The Modelsmentioning

confidence: 99%

“…Other characteristics of TMEV infection that are reflective of MS include immune-mediated (CD4 + and CD8 + T cells) demyelination and pathology [ 146 ]. The presence of antibody, being both produced and deposited within the CNS, is also reflective of what is seen in MS [ 7 , 97 , 131 , 226 ].…”

Section: The Modelsmentioning

confidence: 99%

“…The presence of antibody, being both produced and deposited within the CNS, is also reflective of what is seen in MS [ 7 , 97 , 131 , 226 ]. The TMEV mouse model most closely resembles chronic progressive MS [ 146 ]. For both TMEV and MS, the disease progresses through a significant portion of the animal’s/patient’s life span but then seems to plateau, as the progressive neurological disability does not tend to ultimately cause the death of the animal/person [ 226 ].…”

Section: The Modelsmentioning

confidence: 99%

“…MHV lesions, characterized by focal areas of demyelination of the white matter of the spinal cord with myelin stripping accompanied by naked axons, are histologically very similar to MS lesions [ 82 , 146 , 147 , 227 ]. Also for MHV, both the immune-mediated demyelination and the presence of antibody production within the CNS are reflective of what is seen in MS [ 7 , 105 ].…”

Section: The Modelsmentioning

confidence: 99%

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Viral mouse models used to study multiple sclerosis: past and present

Libbey

Fujinami

2021

Arch Virol

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Multiple sclerosis (MS) is a common inflammatory demyelinating disease of the central nervous system. Although the etiology of MS is unknown, genetics and environmental factors, such as infections, play a role. Viral infections of mice have been used as model systems to study this demyelinating disease of humans. Three viruses that have long been studied in this capacity are Theiler’s murine encephalomyelitis virus, mouse hepatitis virus, and Semliki Forest virus. This review describes the viruses themselves, the infection process, the disease caused by infection and its accompanying pathology, and the model systems and their usefulness in studying MS.

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Section: The Diseasementioning

confidence: 99%

Section: The Modelsmentioning

confidence: 99%

Section: The Modelsmentioning

confidence: 99%

Section: The Modelsmentioning

confidence: 99%

Section: The Modelsmentioning

confidence: 99%

See 3 more Smart Citations

Viral mouse models used to study multiple sclerosis: past and present

Libbey

Fujinami

2021

Arch Virol

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The CD40/CD40 ligand dyad and its downstream effector molecule ISG54 in relating acute neuroinflammation with persistent, progressive demyelination

Hazra,

Das Sarma

2023

IUBMB Life

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Although Multiple Sclerosis (MS) is primarily thought to be an autoimmune condition, its possible viral etiology must be taken into consideration. When mice are administered neurotropic viruses like mouse hepatitis virus MHV‐A59, a murine coronavirus, or its isogenic recombinant strain RSA59, neuroinflammation along with demyelination are observed, which are some of the significant manifestations of MS. MHV‐A59/RSA59 induced neuroinflammation is one of the best‐studied experimental animal models to understand the viral‐induced demyelination concurrent with axonal loss. In this experimental animal model, one of the major immune checkpoint regulators is the CD40‐CD40L dyad, which helps in mediating both acute‐innate, innate‐adaptive, and chronic‐adaptive immune responses. Hence, they are essential in reducing acute neuroinflammation and chronic progressive adaptive demyelination. While CD40 is expressed on antigen‐presenting cells and endothelial cells, CD40L is expressed primarily on activated T cells and during severe inflammation on NK cells and mast cells. Experimental evidences revealed that genetic deficiency of both these proteins can lead to deleterious effects in an individual. On the other hand, interferon‐stimulated genes (ISGs) possess potent antiviral properties and directly or indirectly alter acute neuroinflammation. In this review, we will discuss the role of an ISG, ISG54, and its tetratricopeptide repeat protein Ifit2; the genetic and experimental studies on the role of CD40 and CD40L in a virus‐induced neuroinflammatory demyelination model.

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Post Transplantation Cyclophosphamide Improves Outcome of Autologous Hematopoietic Stem Cell Transplantation in Animal Model of Multiple Sclerosis

Kasarełło

Snarski

Sulejczak

et al. 2021

Arch. Immunol. Ther. Exp.

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Experimental allergic encephalomyelitis (EAE) is the animal model of multiple sclerosis (MS). Autologous hematopoietic stem cell transplantation (AHSCT) has recently been recognized as the standard treatment for MS. The aim of our experiment was to investigate the effect of AHSCT with the addition of low-dose post-transplantation cyclophosphamide (Cy) on EAE in rats. Low dose post-transplantation Cy is used in haploidentical HSCT to reduce the risk of graft versus host disease. We hypothesized that it could bring additional benefit in autologous HSCT in autoimmune diseases. Rats with evoked EAE were treated with high dose (125 mg/kg) Cy, followed by AHSCT or high dose (125 mg/kg) Cy followed by AHSCT followed by low dose (20 mg/kg) Cy in two-time schedules—with the therapy applied during the pre-symptomatic or symptomatic phase of the disease. Both AHSCT and AHSCT with post-transplantation Cy in accordance with both time schedules reduce the intensity of the inflammatory response in the CNS, in comparison with non-treated EAE rats. The reduction of clinical symptoms was present in all AHSCT treatment protocols, however, it was significantly stronger when post-transplantation Cy was given during the symptomatic phase of the disease. AHSCT with the addition of post HSCT low dose Cy improved the results of AHSCT by not only reducing the intensity of inflammation in the CNS but also by significantly reducing the clinical symptoms in treated animals when compared to AHSCT alone. We provide an experimental rationale that the addition of post-transplantation Cy may improve the outcome of HSCT in MS. Graphic Abstract

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Animal Models of Multiple Sclerosis

Cited by 3 publications

References 72 publications

Viral mouse models used to study multiple sclerosis: past and present

Viral mouse models used to study multiple sclerosis: past and present

The CD40/CD40 ligand dyad and its downstream effector molecule ISG54 in relating acute neuroinflammation with persistent, progressive demyelination

Post Transplantation Cyclophosphamide Improves Outcome of Autologous Hematopoietic Stem Cell Transplantation in Animal Model of Multiple Sclerosis

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