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Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...

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DNase hypersensitive sites and association with multiple sclerosis.

Giulio Disanto1, Geir Kjetil Sandve, Vito A G Ricigliano

  • 1Department of Physiology, Anatomy and Genetics and Medical Research Council Functional Genomics Unit, University of Oxford, South Parks Road, Oxford OX1 3PT, UK.

Human Molecular Genetics
|October 5, 2013
PubMed
Summary

Multiple sclerosis (MS) risk is influenced by genetic variants active in immune cells. This study identified T helper 1, T helper 17, cytotoxic T, B, and natural killer cells as key players in MS development.

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Area of Science:

  • Immunology
  • Genetics
  • Neuroscience

Background:

  • Genome-wide association studies (GWASs) have identified approximately 60 genetic variants associated with multiple sclerosis (MS) risk.
  • Understanding the cellular context of these genetic variants is crucial for elucidating MS pathogenesis.

Purpose of the Study:

  • To identify the specific cell types where MS-associated genetic variants are active.
  • To investigate the role of immune cells in the etiology of multiple sclerosis.

Main Methods:

  • Utilized data from MS-associated single nucleotide polymorphisms (SNPs) and deoxyribonuclease I hypersensitive sites (DHSs) across 112 cell types.
  • Employed the Genomic Hyperbrowser for overlap analysis and the GRAIL software to assess gene expression profiles near MS-associated SNPs.

Main Results:

  • Genomic regions associated with MS showed significant enrichment in immune cell DHSs, particularly in T helper 1 (Th1), T helper 17 (Th17), CD8+ cytotoxic T cells, CD19+ B cells, and CD56+ natural killer (NK) cells.
  • New candidate MS-associated genes were identified, including CARD11, FCRL2, CHST12, SYK, TCF7, SOCS1, NFKBIZ, and NPAS1.
  • The immunological profile of regions with suggestive MS association mirrored that of confirmed associations, suggesting many risk variants may not reach genome-wide significance.

Conclusions:

  • Genetic evidence strongly implicates Th1, Th17, cytotoxic T, B, and NK cells in the development of multiple sclerosis.
  • The findings suggest a shared immunological basis for MS and other immune-mediated diseases.
  • Many genetic variants influencing MS risk may not achieve genome-wide significance but are functionally relevant in specific immune cell types.