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Identification of gene regions regulating inflammatory microglial response in the rat CNS after nerve injury

Diez, Margarita; Abdelmagid, Nada; Harnesk, Karin; Strom, Mikael; Lidman, Olle; Swanberg, Maria LU ; Lindblom, Rickard; Al-Nimer, Faiez; Jagodic, Maja and Olsson, Tomas, et al. (2009) In Journal of Neuroimmunology 212(1-2). p.82-92
Abstract
Local CNS inflammation takes place in many neurological disorders and is important for autoimmune neuroinflammation. Microglial activation is strain-dependent in rats and differential MHC class II expression is influenced by variations in the Mhc2ta gene. Despite sharing Mhc2ta and MHC class II alleles, BN and LEW.1N rats differ in MHC class II expression after ventral root avulsion (VRA). We studied MHC class II expression and glial activation markers in BN rats after VRA. Our results demonstrate that MHC class II expression originates from a subpopulation of IBA1(+), ED1(-), and ED2(-) microglia. We subsequently performed a genome-wide linkage scan in an F2(BNxLEW.1N) population, to investigate gene regions regulating this inflammatory... (More)
Local CNS inflammation takes place in many neurological disorders and is important for autoimmune neuroinflammation. Microglial activation is strain-dependent in rats and differential MHC class II expression is influenced by variations in the Mhc2ta gene. Despite sharing Mhc2ta and MHC class II alleles, BN and LEW.1N rats differ in MHC class II expression after ventral root avulsion (VRA). We studied MHC class II expression and glial activation markers in BN rats after VRA. Our results demonstrate that MHC class II expression originates from a subpopulation of IBA1(+), ED1(-), and ED2(-) microglia. We subsequently performed a genome-wide linkage scan in an F2(BNxLEW.1N) population, to investigate gene regions regulating this inflammatory response. Alongside MHC class II, we studied the expression of MHC class 1, costimulatory molecules, complement components, microglial markers and Il1b. MHC class II and other transcripts were commonly regulated by gene regions on chromosomes 1 and 7. Furthermore, a common region on chromosome 10 regulated expression of complement and co-stimulatory molecules, while a region on chromosome II regulated MHC class I. We also detected epistatic interactions in the regulation of the inflammatory process. These results reveal the complex regulation of CNS inflammation by several gene regions, which may have relevance for disease. (C) 2009 Elsevier B.V. All rights reserved. (Less)
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publication status
published
subject
keywords
QTL, Complement, Neuroinflammation, MHC class II, Gene mapping
in
Journal of Neuroimmunology
volume
212
issue
1-2
pages
82 - 92
publisher
Elsevier
external identifiers
  • wos:000268650400010
  • scopus:67649878614
ISSN
1872-8421
DOI
10.1016/j.jneuroim.2009.05.004
language
English
LU publication?
yes
id
ced3ab48-2ea5-4b6e-a163-2738fdb5ac05 (old id 1459912)
date added to LUP
2009-08-31 10:43:06
date last changed
2017-02-22 09:41:12
@article{ced3ab48-2ea5-4b6e-a163-2738fdb5ac05,
  abstract     = {Local CNS inflammation takes place in many neurological disorders and is important for autoimmune neuroinflammation. Microglial activation is strain-dependent in rats and differential MHC class II expression is influenced by variations in the Mhc2ta gene. Despite sharing Mhc2ta and MHC class II alleles, BN and LEW.1N rats differ in MHC class II expression after ventral root avulsion (VRA). We studied MHC class II expression and glial activation markers in BN rats after VRA. Our results demonstrate that MHC class II expression originates from a subpopulation of IBA1(+), ED1(-), and ED2(-) microglia. We subsequently performed a genome-wide linkage scan in an F2(BNxLEW.1N) population, to investigate gene regions regulating this inflammatory response. Alongside MHC class II, we studied the expression of MHC class 1, costimulatory molecules, complement components, microglial markers and Il1b. MHC class II and other transcripts were commonly regulated by gene regions on chromosomes 1 and 7. Furthermore, a common region on chromosome 10 regulated expression of complement and co-stimulatory molecules, while a region on chromosome II regulated MHC class I. We also detected epistatic interactions in the regulation of the inflammatory process. These results reveal the complex regulation of CNS inflammation by several gene regions, which may have relevance for disease. (C) 2009 Elsevier B.V. All rights reserved.},
  author       = {Diez, Margarita and Abdelmagid, Nada and Harnesk, Karin and Strom, Mikael and Lidman, Olle and Swanberg, Maria and Lindblom, Rickard and Al-Nimer, Faiez and Jagodic, Maja and Olsson, Tomas and Piehl, Fredrik},
  issn         = {1872-8421},
  keyword      = {QTL,Complement,Neuroinflammation,MHC class II,Gene mapping},
  language     = {eng},
  number       = {1-2},
  pages        = {82--92},
  publisher    = {Elsevier},
  series       = {Journal of Neuroimmunology},
  title        = {Identification of gene regions regulating inflammatory microglial response in the rat CNS after nerve injury},
  url          = {http://dx.doi.org/10.1016/j.jneuroim.2009.05.004},
  volume       = {212},
  year         = {2009},
}