Identification of gene regions regulating inflammatory microglial response in the rat CNS after nerve injury
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1459912
- author
- organization
- publishing date
- 2009
- type
- Contribution to journal
- 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
- 2016-04-01 12:03:52
- date last changed
- 2022-04-05 17:06:12
@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}}, keywords = {{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}}, doi = {{10.1016/j.jneuroim.2009.05.004}}, volume = {{212}}, year = {{2009}}, }