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Analysis of an interferon- gene dinucleotide-repeat polymorphism in Nordic multiple sclerosis patients

Division of Neurology, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, S-141 86, Stockholm, Sweden

T Masterman

Division of Neurology, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, S-141 86, Stockholm, Sweden

W X Huang

Division of Neurology, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, S-141 86, Stockholm, Sweden

M Sandberg-Wollheim

Department of Neurology, Lund University Hospital, S-221 85, Lund, Sweden

M Laaksonen

Turku Immunology Centre and Department of Virology, University of Turku, FIN-20520 Turku, Finland

H F Harbo

Institute of Transplantation Immunology, Rikshospitalet, N-0027 Oslo, Norway

A Oturai

Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, DK-2100 Copenhagen, Denmark, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, DK-2100 Copenhagen, Denmark

L P Ryder

Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, DK-2100 Copenhagen, Denmark

P Soelberg-Sørensen

Department of Neurology, Copenhagen University Hospital, Rigshospitalet, DK-2100 Copenhagen, Denmark

A Svejgaard

Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, DK-2100 Copenhagen, Denmark

J Hillert

Division of Neurology, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, S-141 86, Stockholm, Sweden

The proinflammatory cytokine interferon (IFN)- has been shown to influence the course of multiple sclerosis (MS). The IFN- (IFNG) contains a multiallelic dinucleotide repeat in intron l. To investigate whether alleles at this locus influence susceptibility to MS, we performed linkage and familial association analyses on 100 sibling pairs from four Nordic countries, and case-control association analysis on 220 intermediately disabled sporadic MS patients and 266 controls. To determine the effect of the polymorphism on disease outcome, we compared genotype frequencies in the most and least disabled octiles of a total cohort of 913 cases. We also measured IFN- mRNA levels in unstimulated peripheral blood mononuclear cells from 46 MS patients and 27 controls grouped according to IFNG intron l genotype. Both nonparametric linkage analysis and transmission disequilibrium testing of the 100 sibling pairs produced negative results. Genotype frequencies for intermediate-MS patients did not differ significantly from those for controls; nor did genotype frequencies in the benign-MS octile differ significantly from those in the severe-MS octile. Comparison of IFN- mRNA levels in genotype-conditioned subgroups revealed no significant differences. Thus, alleles at the IFNG intron l dinucleotide repeat appear to affect neither MS susceptibility and severity nor IFN- mRNA expression in vivo.

Key Words: gene expression • interferon-gamma • linkage • multiple sclerosis • polymorphism • prognosis

Multiple Sclerosis, Vol. 7, No. 3, 157-163 (2001)
DOI: 10.1177/135245850100700304


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