Sequence polymorphisms in the chemokines Scya1 (TCA-3), Scya2 (monocyte chemoattractant protein (MCP)-1), and Scya12 (MCP-5) are candidates for eae7, a locus controlling susceptibility to monophasic remitting/nonrelapsing experimental allergic encephalomyelitis.

摘要: Experimental allergic encephalomyelitis (EAE), the principal animal model of multiple sclerosis, is genetically controlled. To date, 13 disease-modifying loci have been identified in mouse by whole genome scanning using an F2 intercross between EAE-susceptible SJL/J and EAE-resistant B10.S/DvTe mice. Two quantitative trait (QTL), eae6 eae7, on chromosome 11 were classical marker-specific linkage analysis interval mapping. Both QTL reported to be associated with severity duration clinical signs. eae7 was subsequently shown a unique locus controlling development monophasic remitting/nonrelapsing EAE. In this study, composite mapping resolved into two linked QTL: eae6a at 0-13 cM disease severity, eae6b 19-28 Additionally, significantly refined locations eae6a, eae6b, thereby facilitating systematic candidate gene screening cDNA sequencing alleles. Sequence polymorphisms not seen Lif IL12 beta, genes for respectively. Similarly, sequence Nos2, Scya3, Scya4, Scya5, Scya6, Scya7, Scya9, Scya10, Scya11 excluded as candidates eae7. However, resulting significant amino acid substitutions Scya1 (TCA-3), Scya2 (monocyte chemoattractant protein (MCP)-1), Scya12 (MCP-5). Given role chemokines EAE, these are promising signs susceptibility shorter, less severe form disease.