Effects of human recombinant-interferon β in experimental autoimmune encephalomyelitis in guinea pigs

Aritake, Kosuke; Koh, Chang−Sung; Inoue, Akira; Yabuuchi, Fumie; Kitagaki, Kunihiko; Ikoma, Yukihiro; Hayashi, Shigehiro

doi:10.3109/13880201003770135

Pharmaceutical Biology

2010

DOI: 10.3109/13880201003770135

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Effects of human recombinant-interferon β in experimental autoimmune encephalomyelitis in guinea pigs

Kosuke Aritake¹,

Chang−Sung Koh

Akira Inoue

et al.

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Cited by 2 publications

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“…Experimental autoimmune encephalomyelitis (EAE) is an umbrella term referring to multiple different models of CNS autoimmunity in vertebrate animals. Besides rats and mice, these have included species as diverse as non-human primates [4] and guinea pigs [5]. However, the bulk of the literature has centered on the study of CNS autoimmunity in rats and mice, with the latter being the focus of this review.…”

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Using EAE to better understand principles of immune function and autoimmune pathology

Rangachari

Kuchroo

2013

Journal of Autoimmunity

214

156

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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) in which myelin becomes the target of attack by autoreactive T cells. The immune components of the disease are recapitulated in mice using the experimental autoimmune encephalomyelitis (EAE) model. EAE is classically induced by the immunization of mice with encephalitogenic antigens derived from CNS proteins such as proteolipid protein (PLP), myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG). Immunization of susceptible mouse strains with therse antigens will induce autoreactive inflammatory T cell infiltration of the CNS. More recently, the advent of clonal T cell receptor transgenic mice has led to the development of adoptive transfer protocols in which myelin-specific T cells may induce disease upon transfer into naïve recipient animals. When used in concert with gene knockout strains, these protocols are powerful tools by which to dissect the molecular pathways that promote inflammatory T cells responses in the central nervous system (CNS). Further, myelin-antigen-specific transgenic T cells may be cultured in vitro under a variety of conditions prior to adoptive transfer, allowing one to study the effects of soluble factors or pharmacologic compounds on T cell pathogenicity. In this review, we describe many of the existing models of EAE, and discuss the contributions that use of these models has made in understanding both T helper cell differentiation and the function of inhibitory T cell receptors. We focus on the the step-by-step elucidation of the network of signals required for T helper 17 (Th17) cell differentiation, as well as the molecular dissection of the Tim-3 negative regulatory signaling pathway in Th1 cells.

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confidence: 99%

Using EAE to better understand principles of immune function and autoimmune pathology

Rangachari

Kuchroo

2013

Journal of Autoimmunity

214

156

View full text Add to dashboard Cite

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Intranasal interferon beta improves memory and modulates inflammatory responses in a mutant APP-overexpressing rat model of Alzheimer’s disease

Chavoshinezhad

Kouchesfahani

Salehi

et al. 2019

Brain Research Bulletin

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Effects of human recombinant-interferon β in experimental autoimmune encephalomyelitis in guinea pigs

Cited by 2 publications

References 27 publications

Using EAE to better understand principles of immune function and autoimmune pathology

Using EAE to better understand principles of immune function and autoimmune pathology

Intranasal interferon beta improves memory and modulates inflammatory responses in a mutant APP-overexpressing rat model of Alzheimer’s disease

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