Abstract
Evidence for parent-of-origin effects in multiple sclerosis (MS) development and in inheritance of experimental autoimmune encephalomyelitis (EAE), with 1/3 of the risk loci displaying an imprinting-like transmission, strongly suggest epigenetic involvement in MS pathogenesis. Using a whole genome approach, we here sought to identify epigenetically regulated genes that potentially underlie this contribution, in CD4+ T cells, one of the key players in MS disease. To identify imprinted genes, an EAE susceptible rat strain and an EAE resistant rat strain, single nucleotide polymorphisms (SNPs) segregating the two strains, were bred in a reciprocal manner.
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