Modelling MS: Chronic-Relapsing EAE in the NOD/Lt Mouse Strain.

摘要: Modelling complex disorders presents considerable challenges, and multiple sclerosis (MS) is no exception to this rule. The aetiology of MS unknown, its pathophysiology poorly understood. Moreover, the last two decades have witnessed a dramatic revision long-held view as an inflammatory demyelinating white matter disease. Instead, it now regarded global central nervous system (CNS) disorder with neurodegenerative component. Currently, there animal model recapitulating immunopathogenesis. Available models are based on autoimmune-mediated demyelination, denoted experimental autoimmune encephalomyelitis (EAE ) or virally chemically induced demyelination. Of these, EAE has been most commonly used. It extensively improved since first description exists number variants, including genetically modified humanized versions. Nonetheless, distinct disease, each variant only certain facets MS. Whilst search for more refined must continue, important further explore where mechanisms underlying provide proof-of-principle those driving pathogenesis. variants generated myelin component oligodendrocyte glycoprotein (MOG emerged preferred ones, because in particular disease associated both T- B-cell effector mechanisms, together MOG-induced non-obese diabetic (NOD) mouse strain exhibits chronic-relapsing clinical profile high incidence. We describe generation variant, contribution understanding immune pathogenetic potential evaluation candidate therapies.