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The T-cell receptor beta locus and susceptibility to multiple sclerosis

From the University of Cambridge Neurology unit (Drs. Wood, Sawcer, Kellar-Wood, Robertson, and Compston), Addenbrooke's Hospital, Cambridge, UK; MRC Biostatistics Unit (Dr. Holmans and D. Clayton), Institute of Public Health, University Forvie Site, Cambridge, UK; and MRC Cambridge Centre for Brain Repair (Dr. Compston), University Forvie Site, Cambridge, UK.
Supported by the Multiple Sclerosis Society of Great Britain and Northern Ireland.
Received November 29, 1994. Accepted in final form March 1, 1995.
Address correspondence and reprint requests to DrS. Compston, University of Cambridge Neurology unit, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK.

Assessments of genetically determined variations in the T-cell antigen receptor in multiple sclerosis (MS) have yielded conflicting results. We used three restriction fragment length polymorphisms (RFLPs) and a polymorphic microsatellite repeat as markers for the T-cell receptor (TCR) beta locus (7q32-35) in multiplex MS families. Affected sibling-pair analysis of the RFLP data failed to show evidence for linkage (127 families) whereas analysis of the microsatellite data (86 families) provided weak evidence for linkage with a maximum lod score of 0.98 (p less than 0.05). We repeated the analysis in those families (n equals 53) in which the affected sibling pairs were concordant for the HLA haplotype DR15/DQ6. This altered the proportion of affected siblings sharing 0, 1, and 2 RFLP haplotypes from 0.24, 0.50, and 0.26 (p equals NS) before stratification to 0.16, 0.41, and 0.43 (p less than 0.05) in the DR15/DQ6 positive pairs alone; for the microsatellite data, sharing altered from 0.16, 0.50, and 0.34 (p less than 0.05) in all pairs to 0.07, 0.49, and 0.44 (p less than 0.01) in the DR15/DQ6 concordant siblings.

NEUROLOGY 1995;45: 1859-1863

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