Induction of active and adoptive relapsing experimental autoimmune encephalomyelitis (EAE) using an encephalitogenic epitope of proteolipid protein

McRae, Bradford L.; Kennedy, Mark; Tan, Litjen; Canto, Mauro C. Dal; Picha, Kathleen S.; Miller, Stephen D.

doi:10.1016/0165-5728(92)90016-e

Cited by 221 publications

(150 citation statements)

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“…IL-17 producing T lymphocytes known as Th17 cells have recently emerged as a distinct T cell lineage and are the main proinflammatory effector T cells involved in pathogenesis of EAE. Active induction of EAE in mice requires immunization with myelin Ags (proteins or peptides) emulsified in CFA along with pertussis toxin injections [38]. using CD4 + T cells, generally of the T helper phenotype, with Ag specificity for myelin Ags, passive EAE could be induced as well [5].…”

Section: Discussionmentioning

confidence: 99%

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Experimental Autoimmune Encephalomyelitis (EAE) Induced by Antigen Pulsed Dendritic Cells in the C57BL/6 Mouse: Influence of Injection Route

2008

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Section: Discussionmentioning

confidence: 99%

“…EAE is an inflammatory demyelinating disease of the CNS that is induced by immunization of susceptible mice with myelin proteins or peptides [15,38]. In this study, EAE induction in control groups (n=6) was performed using MOG peptide as the encephalitogenic antigen.…”

Section: Eae Induction In C57bl/6 Micementioning

confidence: 99%

Experimental Autoimmune Encephalomyelitis (EAE) Induced by Antigen Pulsed Dendritic Cells in the C57BL/6 Mouse: Influence of Injection Route

2008

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“…3) (a list of these genes is provided in supplemental table 1. 4 ). Notably, the tested specimens segregated according to their corresponding clinical stage with those from disease peak (Fig.…”

Section: Cumulative Expression Profiling In Immunized and Control Micementioning

confidence: 99%

“…By following patterns of gene expression over time in suitable and well-controlled experimental models, it should be possible to identify early pathogenic mechanisms that precede symptoms and to unravel regulatory events undetectable at the clinical or pathological level. Experimental autoimmune encephalomyelitis (EAE) can be induced in a variety of animal species, including nonhuman primates, by active immunization with myelin proteins or their peptide derivatives, as well as by adoptive transfer of activated CD4 ϩ T cells specific for myelin components (1)(2)(3)(4)(5)(6). The encephalitogenic challenge compromises blood-brain barrier (BBB) integrity and produces CNS inflammation and neurodegeneration leading to neurologic disease.…”

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confidence: 99%

Modular Transcriptional Activity Characterizes the Initiation and Progression of Autoimmune Encephalomyelitis

Baranzini

Bernard

Oksenberg

2005

The Journal of Immunology

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Murine experimental autoimmune encephalomyelitis is a well-established model that recapitulates many clinical and physiopathological aspects of multiple sclerosis (MS). An important conceptual development in the understanding of both experimental autoimmune encephalomyelitis and MS pathogenesis has been the compartmentalization of the mechanistic process into two distinct but overlapping and connected phases, inflammatory and neurodegenerative. However, the dynamics of CNS transcriptional changes that underlie the development and regression of the phenotype are not well understood. Our report presents the first high frequency longitudinal study looking at the earliest transcriptional changes in the CNS of NOD mice immunized with myelin oligodendrocyte glycoprotein 35-55 in CFA. Microarray-based gene expression profiling and histopathological analysis were performed from spinal cord samples obtained at 13 time points around the first clinical symptom (every other day until day 11 and every day onward until day 19 postimmunization). Advanced statistics and data-mining algorithms were used to identify expression signatures that correlated with disease stage and histological profiles. Discrete phases of neuroinflammation were accompanied by distinctive expression signatures, in which altered immune to neural gene expression ratios were observed. By using high frequency gene expression analysis we captured expression profiles that were characteristic of the transition from innate to adaptive immune response in this experimental paradigm between days 11 and 12 postimmunization. Our study demonstrates the utility of large-scale transcriptional studies and advanced data mining to decipher complex biological processes such as those involved in MS and other neurodegenerative disoders. The Journal of Immunology, 2005, 174: 7412-7422.C hronic autoimmune diseases like multiple sclerosis (MS) 3 develop over the course of months or years without exhibiting any observable phenotype. By following patterns of gene expression over time in suitable and well-controlled experimental models, it should be possible to identify early pathogenic mechanisms that precede symptoms and to unravel regulatory events undetectable at the clinical or pathological level. Experimental autoimmune encephalomyelitis (EAE) can be induced in a variety of animal species, including nonhuman primates, by active immunization with myelin proteins or their peptide derivatives, as well as by adoptive transfer of activated CD4 ϩ T cells specific for myelin components (1-6). The encephalitogenic challenge compromises blood-brain barrier (BBB) integrity and produces CNS inflammation and neurodegeneration leading to neurologic disease. Ataxia and paralysis occurs first in the tail and hind limbs, and progressive deterioration later affects the forelimbs, eventually causing death. From all available EAE murine models, the one induced by myelin oligodendrocyte glycoprotein (MOG) in the NOD background is perhaps the most adequate for a time-controlled experiment, in ...

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“…Determinantspecific DTH reactions were quantitated as previously described (26 Figure 1. Epitope-mapping pin peptide series for PLP.…”

Section: T Cell Lines and T Cell Assaysmentioning

confidence: 99%

A predictable sequential determinant spreading cascade invariably accompanies progression of experimental autoimmune encephalomyelitis: a basis for peptide-specific therapy after onset of clinical disease.

Johnson

Tuohy

1996

The Journal of Experimental Medicine

256

185

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SummaryThe development of autoimmune disease is accompanied by the acquired recognition of new self-determinants, a process commonly referred to as determinant spreading. In this study, we addressed the question of whether determinant spreading is pathogenic for progression of chronic-relapsing experimental autoimmune encephalomyelitis (EAE), a disease with many similarities to multiple sclerosis (MS). Our approach involved a systematic epitope mapping of responses to myelin proteolipid protein (PLP) as well as assaying responses to known encephalitogenic determinants of myelin basic protein (MBP 87-99) and myelin oligodendrocyte g|yco-protein (MOG 92-106) at various times after induction of EAE in (SWRXSJL)F1 mice immunized with PLP 139-151. We found that the order in which new determinants are recognized during the course of disease follows a predictable sequential pattem. At monthly intervals after immunization with p139-151, responses to PLP 249-273, MBP 87-99, and PLP 173-198 were sequentially accumulated in all mice examined. Three lines of evidence showed that determinant spreading is pathogenic for disease progression: (a) spreading determinants mediate passive transfer of acute EAE in naive (S'W~• 1 recipients; (b) an invariant relationship exists between the development of relapse/progression and the spreading of recognition to new immunodominant encephalitogenic determinants; and (c) after EAE onset, the induction ofpeptidespecific tolerance to spreading but not to nonspreading encephalitogenic determinants prevents subsequent progression of EAE. Thus, the predictability of acquired self-determinant recognition provides a basis for sequential determinant-specific therapeutic intervention after onset of the autoimmune disease process.

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Induction of active and adoptive relapsing experimental autoimmune encephalomyelitis (EAE) using an encephalitogenic epitope of proteolipid protein

Cited by 221 publications

References 40 publications

Experimental Autoimmune Encephalomyelitis (EAE) Induced by Antigen Pulsed Dendritic Cells in the C57BL/6 Mouse: Influence of Injection Route

Experimental Autoimmune Encephalomyelitis (EAE) Induced by Antigen Pulsed Dendritic Cells in the C57BL/6 Mouse: Influence of Injection Route

Modular Transcriptional Activity Characterizes the Initiation and Progression of Autoimmune Encephalomyelitis

A predictable sequential determinant spreading cascade invariably accompanies progression of experimental autoimmune encephalomyelitis: a basis for peptide-specific therapy after onset of clinical disease.

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