Co-localization of differentially expressed genes and shared susceptibility loci in human autoimmunity

Thomas M. Aune, Joel S. Parker, Kevin Maas, Zheng Liu, Nancy Olsen, Jason H. Moore

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Autoimmune diseases arise from complex interactions between environmental and genetic factors. Genetic linkage scans show that different autoimmune diseases share overlapping susceptibility loci. Lymphocytes from individuals with different autoimmune diseases, as well as unaffected first-degree relatives, also share a common gene expression profile. We sought to determine if genes within this autoimmune expression profile were nonrandomly distributed in the genome and if their distribution overlapped with shared disease susceptibility loci. We found that differentially expressed genes were distributed in a nonrandom fashion in chromosomal domains within the genome. Furthermore, positions of these domains were not statistically different from a number of shared autoimmune disease susceptibility loci. To our knowledge, this is the first study showing concordance between gene expression and genetic linkage results in common complex multifactorial human diseases.

Original languageEnglish (US)
Pages (from-to)162-172
Number of pages11
JournalGenetic Epidemiology
Volume27
Issue number2
DOIs
StatePublished - Sep 1 2004

Fingerprint

Autoimmunity
Autoimmune Diseases
Genetic Linkage
Disease Susceptibility
Genes
Genome
Transcriptome
Lymphocytes
Gene Expression

All Science Journal Classification (ASJC) codes

  • Epidemiology
  • Genetics(clinical)

Cite this

Aune, Thomas M. ; Parker, Joel S. ; Maas, Kevin ; Liu, Zheng ; Olsen, Nancy ; Moore, Jason H. / Co-localization of differentially expressed genes and shared susceptibility loci in human autoimmunity. In: Genetic Epidemiology. 2004 ; Vol. 27, No. 2. pp. 162-172.
@article{b8436389052a4897967eb1a7f0e61078,
title = "Co-localization of differentially expressed genes and shared susceptibility loci in human autoimmunity",
abstract = "Autoimmune diseases arise from complex interactions between environmental and genetic factors. Genetic linkage scans show that different autoimmune diseases share overlapping susceptibility loci. Lymphocytes from individuals with different autoimmune diseases, as well as unaffected first-degree relatives, also share a common gene expression profile. We sought to determine if genes within this autoimmune expression profile were nonrandomly distributed in the genome and if their distribution overlapped with shared disease susceptibility loci. We found that differentially expressed genes were distributed in a nonrandom fashion in chromosomal domains within the genome. Furthermore, positions of these domains were not statistically different from a number of shared autoimmune disease susceptibility loci. To our knowledge, this is the first study showing concordance between gene expression and genetic linkage results in common complex multifactorial human diseases.",
author = "Aune, {Thomas M.} and Parker, {Joel S.} and Kevin Maas and Zheng Liu and Nancy Olsen and Moore, {Jason H.}",
year = "2004",
month = "9",
day = "1",
doi = "10.1002/gepi.20013",
language = "English (US)",
volume = "27",
pages = "162--172",
journal = "Genetic Epidemiology",
issn = "0741-0395",
publisher = "Wiley-Liss Inc.",
number = "2",

}

Co-localization of differentially expressed genes and shared susceptibility loci in human autoimmunity. / Aune, Thomas M.; Parker, Joel S.; Maas, Kevin; Liu, Zheng; Olsen, Nancy; Moore, Jason H.

In: Genetic Epidemiology, Vol. 27, No. 2, 01.09.2004, p. 162-172.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Co-localization of differentially expressed genes and shared susceptibility loci in human autoimmunity

AU - Aune, Thomas M.

AU - Parker, Joel S.

AU - Maas, Kevin

AU - Liu, Zheng

AU - Olsen, Nancy

AU - Moore, Jason H.

PY - 2004/9/1

Y1 - 2004/9/1

N2 - Autoimmune diseases arise from complex interactions between environmental and genetic factors. Genetic linkage scans show that different autoimmune diseases share overlapping susceptibility loci. Lymphocytes from individuals with different autoimmune diseases, as well as unaffected first-degree relatives, also share a common gene expression profile. We sought to determine if genes within this autoimmune expression profile were nonrandomly distributed in the genome and if their distribution overlapped with shared disease susceptibility loci. We found that differentially expressed genes were distributed in a nonrandom fashion in chromosomal domains within the genome. Furthermore, positions of these domains were not statistically different from a number of shared autoimmune disease susceptibility loci. To our knowledge, this is the first study showing concordance between gene expression and genetic linkage results in common complex multifactorial human diseases.

AB - Autoimmune diseases arise from complex interactions between environmental and genetic factors. Genetic linkage scans show that different autoimmune diseases share overlapping susceptibility loci. Lymphocytes from individuals with different autoimmune diseases, as well as unaffected first-degree relatives, also share a common gene expression profile. We sought to determine if genes within this autoimmune expression profile were nonrandomly distributed in the genome and if their distribution overlapped with shared disease susceptibility loci. We found that differentially expressed genes were distributed in a nonrandom fashion in chromosomal domains within the genome. Furthermore, positions of these domains were not statistically different from a number of shared autoimmune disease susceptibility loci. To our knowledge, this is the first study showing concordance between gene expression and genetic linkage results in common complex multifactorial human diseases.

UR - http://www.scopus.com/inward/record.url?scp=4344691958&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4344691958&partnerID=8YFLogxK

U2 - 10.1002/gepi.20013

DO - 10.1002/gepi.20013

M3 - Article

C2 - 15305332

AN - SCOPUS:4344691958

VL - 27

SP - 162

EP - 172

JO - Genetic Epidemiology

JF - Genetic Epidemiology

SN - 0741-0395

IS - 2

ER -