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Volume 288, Issue 1, Pages 63-67 (15 January 2010)


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Presence of CSF oligoclonal bands (OCB) is associated with the HLA-DRB1 genotype in a West Australian multiple sclerosis cohort

Jing-Shan Wua, Wei Qiuae, Alison Castleyb, Ian Jamesc, Joyce Josepha, Frank T Christiansenbd, William M Carrolla, Frank L Mastagliaa, Allan G KermodeaCorresponding Author Informationemail address

Received 27 July 2009; received in revised form 5 October 2009; accepted 7 October 2009. published online 02 November 2009.

Abstract 

High-resolution HLA-DRB1 genotyping was performed in 97 OCB-positive and 68 OCB-negative cases with demyelinating disease to determine the influence of HLA-DRB1 alleles on the presence of OCB in a West Australian multiple sclerosis (MS) cohort. Carriage of the HLA-DRB1*1501 allele was associated with both OCB-positive and OCB-negative MS compared with controls, but more strongly with the OCB-positive group, and increased the likelihood of having OCB 2.1-fold with evidence of a dominant dose–effect. The HLA-DRB1*0301 allele was negatively correlated with OCB, with all homozygotes OCB-negative, suggesting a possible recessive protective effect of HLA-DRB1*0301. There was no significant correlation between OCB and the DRB1*04 alleles which have been associated with OCB-negative MS in previous Swedish and Japanese studies. Evidence of allelic interactions was found with HLA-DRB1*1501/*1301 heterozygotes having a reduced frequency of OCB and HLA-DRB1*0301/*0401 heterozygotes all being OCB-negative. These findings confirm the strong association between HLA-DRB1*1501 and OCB which has been found in other populations but indicate that the influence of other HLA-DRB1 alleles varies in different populations. Our study is the first to show that HLA-DRB1 allele interactions and dose–effects influence the frequency of OCB.

a Australian Neuromuscular Research Institute, Sir Charles Gairdner Hospital; Centre for Neuromuscular and Neurological Disorders, University of Western Australia, Queen Elizabeth II Medical Centre, 6009, Perth, WA, Australia

b Department of Clinical Immunology and Immunogenetics, PathWest Royal Perth Hospital, Perth, Western Australia, Australia

c Centre for Clinical Immunology & Biomedical Statistics, Murdoch University & Royal Perth Hospital, Perth, Western Australia, Australia

d School of Pathology and Laboratory Medicine, University of Western Australia, Perth, Western Australia, Australia

e Department of Neurology, the Third Affiliated Hospital of Sun Yet-sen University, Guangzhou, China

Corresponding Author InformationCorresponding author. Tel.: +61 8 93881865; fax: +61 8 93882149.

PII: S0022-510X(09)00901-0

doi:10.1016/j.jns.2009.10.005


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