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Gene expression profile in multiple sclerosis patients and healthy controls: identifying pathways relevant to disease

Bomprezzi, R; Ringnér, Markus LU ; Kim, S; Bittner, ML; Khan, J; Chen, YD; Elkahloun, A; Yu, AM; Bielekova, B and Meltzer, PS, et al. (2003) In Human Molecular Genetics 12(17). p.2191-2199
Abstract
Multiple sclerosis (MS) and other T cell-mediated autoimmune diseases develop in individuals carrying a complex susceptibility trait, probably following exposure to various environmental triggers. Owing to the presumed weak influence of single genes on disease predisposition and the recognized genetic heterogeneity of autoimmune disorders in humans, candidate gene searches in MS have been difficult. In an attempt to identify molecular markers indicative of disease status rather than susceptibility genes for MS, we show that gene expression profiling of peripheral blood mononuclear cells by cDNA microarrays can distinguish MS patients from healthy controls. Our findings support the concept that the activation of autoreactive T cells is of... (More)
Multiple sclerosis (MS) and other T cell-mediated autoimmune diseases develop in individuals carrying a complex susceptibility trait, probably following exposure to various environmental triggers. Owing to the presumed weak influence of single genes on disease predisposition and the recognized genetic heterogeneity of autoimmune disorders in humans, candidate gene searches in MS have been difficult. In an attempt to identify molecular markers indicative of disease status rather than susceptibility genes for MS, we show that gene expression profiling of peripheral blood mononuclear cells by cDNA microarrays can distinguish MS patients from healthy controls. Our findings support the concept that the activation of autoreactive T cells is of primary importance for this complex organ-specific disorder and prompt further investigations on gene expression in peripheral blood cells aimed at characterizing disease phenotypes. (Less)
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type
Contribution to journal
publication status
published
subject
in
Human Molecular Genetics
volume
12
issue
17
pages
2191 - 2199
publisher
Oxford University Press
external identifiers
  • wos:000185321300010
  • pmid:12915464
  • scopus:10744231299
ISSN
0964-6906
DOI
10.1093/hmg/ddg221
language
English
LU publication?
yes
id
b35a5845-3d75-44a1-8674-fc1c6429e419 (old id 301306)
date added to LUP
2007-08-24 12:56:51
date last changed
2018-01-14 03:25:25
@article{b35a5845-3d75-44a1-8674-fc1c6429e419,
  abstract     = {Multiple sclerosis (MS) and other T cell-mediated autoimmune diseases develop in individuals carrying a complex susceptibility trait, probably following exposure to various environmental triggers. Owing to the presumed weak influence of single genes on disease predisposition and the recognized genetic heterogeneity of autoimmune disorders in humans, candidate gene searches in MS have been difficult. In an attempt to identify molecular markers indicative of disease status rather than susceptibility genes for MS, we show that gene expression profiling of peripheral blood mononuclear cells by cDNA microarrays can distinguish MS patients from healthy controls. Our findings support the concept that the activation of autoreactive T cells is of primary importance for this complex organ-specific disorder and prompt further investigations on gene expression in peripheral blood cells aimed at characterizing disease phenotypes.},
  author       = {Bomprezzi, R and Ringnér, Markus and Kim, S and Bittner, ML and Khan, J and Chen, YD and Elkahloun, A and Yu, AM and Bielekova, B and Meltzer, PS and Martin, R and McFarland, HF and Trent, JM},
  issn         = {0964-6906},
  language     = {eng},
  number       = {17},
  pages        = {2191--2199},
  publisher    = {Oxford University Press},
  series       = {Human Molecular Genetics},
  title        = {Gene expression profile in multiple sclerosis patients and healthy controls: identifying pathways relevant to disease},
  url          = {http://dx.doi.org/10.1093/hmg/ddg221},
  volume       = {12},
  year         = {2003},
}