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Drug Discov Today. 2014 Sep;19(9):1394-401. doi: 10.1016/j.drudis.2014.03.023. Epub 2014 Apr 2.

Improvement of preclinical animal models for autoimmune-mediated disorders via reverse translation of failed therapies.

Author information

1
Biomedical Primate Research Centre, Department of Immunobiology, Rijswijk, The Netherlands; University of Groningen, Department of Neuroscience, University Medical Center, Groningen, The Netherlands; MS Center ErasMS, Rotterdam, The Netherlands. Electronic address: hart@bprc.nl.
2
Biomedical Primate Research Centre, Department of Immunobiology, Rijswijk, The Netherlands; MS Center ErasMS, Rotterdam, The Netherlands.
3
Biomedical Primate Research Centre, Department of Immunobiology, Rijswijk, The Netherlands; MS Center ErasMS, Rotterdam, The Netherlands; Erasmus Medical Center Rotterdam, Department of Immunology, Rotterdam, The Netherlands.
4
Biomedical Primate Research Centre, Department of Immunobiology, Rijswijk, The Netherlands.
5
MIRCen, CEA, Fontenay-aux-Roses, France.
6
Department of Animal Science, Biomedical Primate Research Centre, 2288 GJ Rijswijk, The Netherlands.

Abstract

The poor translational validity of autoimmune-mediated inflammatory disease (AIMID) models in inbred and specific pathogen-free (SPF) rodents underlies the high attrition of new treatments for the corresponding human disease. Experimental autoimmune encephalomyelitis (EAE) is a frequently used preclinical AIMID model. We discuss here how crucial information needed for the innovation of current preclinical models can be obtained from postclinical analysis of the nonhuman primate EAE model, highlighting the mechanistic reasons why some therapies fail and others succeed. These new insights can also help identify new targets for treatment.

PMID:
24704460
DOI:
10.1016/j.drudis.2014.03.023
[Indexed for MEDLINE]

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