Abstract
Recently, several non-HLA loci have been shown to be convincingly associated with Multiple Sclerosis (MS) susceptibility, assumingly indicating important pathways in the pathogenesis. A genotype influence on disease outcome measures by these genes would support a role of these pathways in ongoing tissue damage. Here, however, we report a consistent dissociation between causation and progression for five non-HLA genotypes (IL7R, IL2RA, CLEC16A, CD226 and SH2B3) in 1776 Scandinavian MS patients.
Copyright © 2011 Elsevier B.V. All rights reserved.
MeSH terms
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Adaptor Proteins, Signal Transducing
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Adult
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Antigens, Differentiation, T-Lymphocyte / genetics
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Antigens, Differentiation, T-Lymphocyte / immunology
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Antigens, Surface / genetics*
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Antigens, Surface / immunology*
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Disease Progression
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Female
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Genetic Predisposition to Disease / ethnology
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Genetic Predisposition to Disease / genetics*
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HLA Antigens / immunology
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Humans
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Interleukin-2 Receptor alpha Subunit / genetics
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Interleukin-2 Receptor alpha Subunit / immunology
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Intracellular Signaling Peptides and Proteins
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Lectins, C-Type / genetics
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Lectins, C-Type / immunology
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Male
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Monosaccharide Transport Proteins / genetics
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Monosaccharide Transport Proteins / immunology
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Multiple Sclerosis / genetics*
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Multiple Sclerosis / immunology*
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Multiple Sclerosis / pathology
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Norway / epidemiology
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Proteins / genetics
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Proteins / immunology
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Receptors, Interleukin-7 / genetics
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Receptors, Interleukin-7 / immunology
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Sweden / epidemiology
Substances
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Adaptor Proteins, Signal Transducing
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Antigens, Differentiation, T-Lymphocyte
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Antigens, Surface
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CD226 antigen
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CLEC16A protein, human
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HLA Antigens
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IL2RA protein, human
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Interleukin-2 Receptor alpha Subunit
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Intracellular Signaling Peptides and Proteins
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Lectins, C-Type
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Monosaccharide Transport Proteins
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Proteins
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Receptors, Interleukin-7
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SH2B3 protein, human