Publication

Merits and complexities of modeling multiple sclerosis in non-human primates: Implications for drug discovery

't Hart, B. A., Laman, J. D. & Kap, Y. S., 2018, In : Expert Opinion on Drug Discovery. 13, 5, p. 387-397 11 p.

Research output: Contribution to journalReview articleAcademicpeer-review

APA

't Hart, B. A., Laman, J. D., & Kap, Y. S. (2018). Merits and complexities of modeling multiple sclerosis in non-human primates: Implications for drug discovery. Expert Opinion on Drug Discovery, 13(5), 387-397. https://doi.org/10.1080/17460441.2018.1443075

Author

't Hart, Bert A. ; Laman, Jon D. ; Kap, Yolanda S. / Merits and complexities of modeling multiple sclerosis in non-human primates : Implications for drug discovery. In: Expert Opinion on Drug Discovery. 2018 ; Vol. 13, No. 5. pp. 387-397.

Harvard

't Hart, BA, Laman, JD & Kap, YS 2018, 'Merits and complexities of modeling multiple sclerosis in non-human primates: Implications for drug discovery', Expert Opinion on Drug Discovery, vol. 13, no. 5, pp. 387-397. https://doi.org/10.1080/17460441.2018.1443075

Standard

Merits and complexities of modeling multiple sclerosis in non-human primates : Implications for drug discovery. / 't Hart, Bert A.; Laman, Jon D.; Kap, Yolanda S.

In: Expert Opinion on Drug Discovery, Vol. 13, No. 5, 2018, p. 387-397.

Research output: Contribution to journalReview articleAcademicpeer-review

Vancouver

't Hart BA, Laman JD, Kap YS. Merits and complexities of modeling multiple sclerosis in non-human primates: Implications for drug discovery. Expert Opinion on Drug Discovery. 2018;13(5):387-397. https://doi.org/10.1080/17460441.2018.1443075


BibTeX

@article{eb6ce9496ea14555b4e25e95a0990308,
title = "Merits and complexities of modeling multiple sclerosis in non-human primates: Implications for drug discovery",
abstract = "Introduction: The translation of scientific discoveries made in animal models into effective treatments for patients often fails, indicating that currently used disease models in preclinical research are insufficiently predictive for clinical success. An often-used model in the preclinical research of autoimmune neurological diseases, multiple sclerosis in particular, is experimental autoimmune encephalomyelitis (EAE). Most EAE models are based on genetically susceptible inbred/SPF mouse strains used at adolescent age (10-12weeks), which lack exposure to genetic and microbial factors which shape the human immune system.Areas covered: Herein, the authors ask whether an EAE model in adult non-human primates from an outbred conventionally-housed colony could help bridge the translational gap between rodent EAE models and MS patients. Particularly, the authors discuss a novel and translationally relevant EAE model in common marmosets (Callithrix jacchus) that shares remarkable pathological similarity with MS.Expert opinion: The MS-like pathology in this model is caused by the interaction of effector memory T cells with B cells infected with the 1-herpesvirus (CalHV3), both present in the pathogen-educated marmoset immune repertoire. The authors postulate that depletion of only the small subset (",
keywords = "Experimental autoimmune encephalomyelitis, animal model, marmoset, translational research, immunotherapy, B cell, EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS, B-CELL DEPLETION, MYELIN OLIGODENDROCYTE GLYCOPROTEIN, CENTRAL-NERVOUS-SYSTEM, CD8(+) T-CELLS, COMMON MARMOSETS, HUMAN IMMUNOLOGY, ANIMAL-MODELS, EBV INFECTION, DOUBLE-BLIND",
author = "{'t Hart}, {Bert A.} and Laman, {Jon D.} and Kap, {Yolanda S.}",
year = "2018",
doi = "10.1080/17460441.2018.1443075",
language = "English",
volume = "13",
pages = "387--397",
journal = "Expert Opinion on Drug Discovery",
issn = "1746-0441",
publisher = "Taylor & Francis Group",
number = "5",

}

RIS

TY - JOUR

T1 - Merits and complexities of modeling multiple sclerosis in non-human primates

T2 - Implications for drug discovery

AU - 't Hart, Bert A.

AU - Laman, Jon D.

AU - Kap, Yolanda S.

PY - 2018

Y1 - 2018

N2 - Introduction: The translation of scientific discoveries made in animal models into effective treatments for patients often fails, indicating that currently used disease models in preclinical research are insufficiently predictive for clinical success. An often-used model in the preclinical research of autoimmune neurological diseases, multiple sclerosis in particular, is experimental autoimmune encephalomyelitis (EAE). Most EAE models are based on genetically susceptible inbred/SPF mouse strains used at adolescent age (10-12weeks), which lack exposure to genetic and microbial factors which shape the human immune system.Areas covered: Herein, the authors ask whether an EAE model in adult non-human primates from an outbred conventionally-housed colony could help bridge the translational gap between rodent EAE models and MS patients. Particularly, the authors discuss a novel and translationally relevant EAE model in common marmosets (Callithrix jacchus) that shares remarkable pathological similarity with MS.Expert opinion: The MS-like pathology in this model is caused by the interaction of effector memory T cells with B cells infected with the 1-herpesvirus (CalHV3), both present in the pathogen-educated marmoset immune repertoire. The authors postulate that depletion of only the small subset (

AB - Introduction: The translation of scientific discoveries made in animal models into effective treatments for patients often fails, indicating that currently used disease models in preclinical research are insufficiently predictive for clinical success. An often-used model in the preclinical research of autoimmune neurological diseases, multiple sclerosis in particular, is experimental autoimmune encephalomyelitis (EAE). Most EAE models are based on genetically susceptible inbred/SPF mouse strains used at adolescent age (10-12weeks), which lack exposure to genetic and microbial factors which shape the human immune system.Areas covered: Herein, the authors ask whether an EAE model in adult non-human primates from an outbred conventionally-housed colony could help bridge the translational gap between rodent EAE models and MS patients. Particularly, the authors discuss a novel and translationally relevant EAE model in common marmosets (Callithrix jacchus) that shares remarkable pathological similarity with MS.Expert opinion: The MS-like pathology in this model is caused by the interaction of effector memory T cells with B cells infected with the 1-herpesvirus (CalHV3), both present in the pathogen-educated marmoset immune repertoire. The authors postulate that depletion of only the small subset (

KW - Experimental autoimmune encephalomyelitis

KW - animal model

KW - marmoset

KW - translational research

KW - immunotherapy

KW - B cell

KW - EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS

KW - B-CELL DEPLETION

KW - MYELIN OLIGODENDROCYTE GLYCOPROTEIN

KW - CENTRAL-NERVOUS-SYSTEM

KW - CD8(+) T-CELLS

KW - COMMON MARMOSETS

KW - HUMAN IMMUNOLOGY

KW - ANIMAL-MODELS

KW - EBV INFECTION

KW - DOUBLE-BLIND

U2 - 10.1080/17460441.2018.1443075

DO - 10.1080/17460441.2018.1443075

M3 - Review article

VL - 13

SP - 387

EP - 397

JO - Expert Opinion on Drug Discovery

JF - Expert Opinion on Drug Discovery

SN - 1746-0441

IS - 5

ER -

ID: 55024916