Production of IL-1beta and IL-1Ra as risk factors for susceptibility and progression of relapse-onset multiple sclerosis

Interleukin-1beta (IL-1beta) is present in multiple sclerosis (MS) lesions. Interleukin-1 receptor antagonist (IL-1Ra) moderates the induction of experimental autoimmune encephalomyelitis (EAE). Here, we show that families that are characterized by high IL-1beta over IL-1Ra production ratio are at 2...

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Bibliographic Details
Published in:Journal of neuroimmunology 2002-05, Vol.126 (1-2), p.172-179
Main Authors: de Jong, Brigit A, Huizinga, Tom W J, Bollen, Eduard L E M, Uitdehaag, Bernard M J, Bosma, Gerlof P Th, van Buchem, Mark A, Remarque, Edmond J, Burgmans, Alexandra C S, Kalkers, Nynke F, Polman, Chris H, Westendorp, Rudi G J
Format: Article
Language:English
Subjects:
Adult
Aged
Disease Progression
Exons
Female
Genetic Predisposition to Disease
HLA-DR Antigens - genetics
HLA-DRB1 Chains
Humans
Interleukin 1 Receptor Antagonist Protein
Interleukin-1 - genetics
Male
Middle Aged
Multiple Sclerosis, Relapsing-Remitting - epidemiology
Multiple Sclerosis, Relapsing-Remitting - genetics
Multiple Sclerosis, Relapsing-Remitting - immunology
Polymorphism, Genetic
Risk Factors
Sialoglycoproteins - genetics
Tandem Repeat Sequences
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Summary:Interleukin-1beta (IL-1beta) is present in multiple sclerosis (MS) lesions. Interleukin-1 receptor antagonist (IL-1Ra) moderates the induction of experimental autoimmune encephalomyelitis (EAE). Here, we show that families that are characterized by high IL-1beta over IL-1Ra production ratio are at 2.2-fold (95% CI, 1.0-4.8; p=0.05) increased risk to have a patient relative with relapse-onset MS than families with a low ratio. It is also related to the reduction of volumetric magnetization transfer ratio (MTR) histogram height, a measure of parenchymal integrity (p=0.04). Those families who combine a high IL-1beta over IL-1Ra ratio with a high tumor necrosis factor (TNF) over IL-10 production ratio have a 6.2-fold (95% CI, 1.8-21; p=0.002) increased risk. Innate production of IL-1beta and IL-1Ra is not related to the outcome of primary progressive MS. Taq1 polymorphism in the IL-1beta gene and the variable number of tandem repeats (VNTR) polymorphism of 86-base pairs within the IL-1Ra gene cannot explain these findings.
ISSN:0165-5728