TY - JOUR
T1 - Gene-expression profiling of experimental autoimmune encephalomyelitis
AU - Mix, Eilhard
AU - Pahnke, Jens
AU - Ibrahim, Saleh M.
N1 - Funding Information:
The work was supported by grants from the German Federal Ministry of Education and Research (BMBF) program NBL3, 01 ZZ0108, to S.M.I. The authors would like to thank colleagues who contributed to the original published experiments namely Tobias Boettcher, Ralf Gold, Dirk Koczan, Arndt Rolfs, and Hans-Juergen Thiesen. We would also like to thank I. Klamfuß for excellent technical assistance and A. Mueller for help with the manuscript.
PY - 2002/10/1
Y1 - 2002/10/1
N2 - Experimental autoimmune encephalomyelitis (EAE) is a mouse model that serves as an experimental tool for studying the etiology, pathogenesis, as well as new therapeutic approaches of multiple sclerosis (MS). EAE is a polygenic chronic inflammatory demyelinating disease of the nervous system that involves the interaction between genetic and environmental factors. Previous studies have identified multiple quantitative trait loci (QTL) controlling different aspects of disease pathogenesis. However, progress in identifying new susceptibility genes outside the MHC locus has been slow. With the advent of new global methods for genetic analysis such as large-scale sequencing, gene expression profiling combined with classic linkage analysis and congenic and physical mapping progress is considerably accelerating. Here we review our preliminary work on the use of gene expression mapping to identify new putative genetic pathways contributing to the pathogenesis of EAE.
AB - Experimental autoimmune encephalomyelitis (EAE) is a mouse model that serves as an experimental tool for studying the etiology, pathogenesis, as well as new therapeutic approaches of multiple sclerosis (MS). EAE is a polygenic chronic inflammatory demyelinating disease of the nervous system that involves the interaction between genetic and environmental factors. Previous studies have identified multiple quantitative trait loci (QTL) controlling different aspects of disease pathogenesis. However, progress in identifying new susceptibility genes outside the MHC locus has been slow. With the advent of new global methods for genetic analysis such as large-scale sequencing, gene expression profiling combined with classic linkage analysis and congenic and physical mapping progress is considerably accelerating. Here we review our preliminary work on the use of gene expression mapping to identify new putative genetic pathways contributing to the pathogenesis of EAE.
UR - http://www.scopus.com/inward/record.url?scp=0036808581&partnerID=8YFLogxK
U2 - 10.1023/A:1020925425780
DO - 10.1023/A:1020925425780
M3 - Journal articles
C2 - 12462414
AN - SCOPUS:0036808581
SN - 0364-3190
VL - 27
SP - 1157
EP - 1163
JO - Neurochemical Research
JF - Neurochemical Research
IS - 10
ER -
