Abstract
Aging Western societies are facing an increasing prevalence of chronic autoimmune-mediated inflammatory disorders (AIMIDs) for which treatments that are safe and effective are scarce. One of the main reasons for this situation is the lack of animal models, which accurately replicate clinical and pathological aspects of the human diseases. One important AIMID is the neuroinflammatory disease multiple sclerosis (MS), for which the mouse experimental autoimmune encephalomyelitis (EAE) model has been frequently used in preclinical research. Despite some successes, there is a long list of experimental treatments that have failed to reproduce promising effects observed in murine EAE models when they were tested in the clinic. This frustrating situation indicates a wide validity gap between mouse EAE and MS. This monography describes the development of an EAE model in nonhuman primates, which may help to bridge the gap.
Highlights
Aging Western societies are facing a steadily increasing prevalence of autoimmune-mediated inflammatory disorders (AIMIDs), for which no effective treatments exist, such as multiple sclerosis (MS) and type I diabetes
While B cells were for a long time viewed only as producers of myelin opsonizing antibodies, which induce demyelination via complement- (CDC) or macrophage-dependent (ADCC) cytotoxicity reactions, they www.primate-biol.net/6/17/2019/
Much is expected from treatment with stem cells (SCs), which are available in different flavors, such as hemopoietic SCs, neural stem/precursor cells (NPCs), mesenchymal SCs or induced pluripotent stem cells (Martino et al, 2010; Di Ruscio et al, 2015)
Summary
Aging Western societies are facing a steadily increasing prevalence of autoimmune-mediated inflammatory disorders (AIMIDs), for which no effective treatments exist, such as MS and type I diabetes. Funding for research aiming at understanding the reasons why treatments developed via forward translation (from the laboratory to the clinic) fail is limited This is an unfortunate situation, as much can be learned from reverse translation research (from the clinic back to the laboratory) and the new insights can be used to improve currently used animal models (’t Hart et al, 2014). The decisive influence of gut microbiota on EAE susceptibility is illustrated in studies by Berer et al, who showed that EAE-prone transgenic mice, which do not develop evident disease under germ-free conditions, become spontaneously sick after administration of normal commensal gut microbiota (Berer et al, 2011). The fact that in nonhuman primates, autoimmune reactions develop within a pathogen-trained immune context marks an important difference with the situation in immunologically naïve inbred/SPF mice
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