Advanced

Finemapping of the arthritis QTL Pia7 reveals co-localization with Oia2 and the APLEC locus.

Rintisch, Carola LU ; Kelkka, T; Norin, U; Lorentzen, J C; Olofsson, P and Holmdahl, Rikard LU (2010) In Genes and Immunity Apr 7. p.239-245
Abstract
In this study, we sought to determine the effect of the quantitative trait locus Pia7 on arthritis severity. The regulatory locus derived from the arthritis-resistant E3 rat strain was introgressed into the arthritis-susceptibility DA strain through continuous backcrossing. Congenic rats were studied for their susceptibility to experimental arthritis using pristane and adjuvant oil. In addition, cell number and function of various leukocyte populations were analyzed either under naive or stimulated conditions. We found that the minimal congenic fragment of DA.E3-Pia7 rats overlapped with the minimal fragment in DA.PVG-Oia2 congenic rats, which has been positionally cloned to the antigen-presenting lectin-like receptor complex (APLEC)... (More)
In this study, we sought to determine the effect of the quantitative trait locus Pia7 on arthritis severity. The regulatory locus derived from the arthritis-resistant E3 rat strain was introgressed into the arthritis-susceptibility DA strain through continuous backcrossing. Congenic rats were studied for their susceptibility to experimental arthritis using pristane and adjuvant oil. In addition, cell number and function of various leukocyte populations were analyzed either under naive or stimulated conditions. We found that the minimal congenic fragment of DA.E3-Pia7 rats overlapped with the minimal fragment in DA.PVG-Oia2 congenic rats, which has been positionally cloned to the antigen-presenting lectin-like receptor complex (APLEC) genes. DA.E3-Pia7 congenic rats were protected from both PIA and OIA, but the protection was more pronounced in OIA. In adoptive transfer experiments we observed that the Pia7 locus controlled the priming of arthritogenic T cells and not the effector phase. In addition, Pia7 congenic rats had a significant higher frequency of B cells and granulocytes as well as TNFalpha production after stimulation, indicating a higher activation state of cells of the innate immune system. In conclusion, this study shows that the APLEC locus is a major locus regulating the severity of experimentally induced arthritis in rats.Genes and Immunity advance online publication, 4 March 2010; doi:10.1038/gene.2010.2. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Genes and Immunity
volume
Apr 7
pages
239 - 245
publisher
Nature Publishing Group
external identifiers
  • wos:000276952300005
  • pmid:20200546
  • scopus:77951499167
ISSN
1476-5470
DOI
10.1038/gene.2010.2
language
English
LU publication?
yes
id
389ad7c8-6d1b-4094-98d3-94e153241d71 (old id 1582573)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20200546?dopt=Abstract
date added to LUP
2010-04-07 14:18:03
date last changed
2018-05-29 09:28:14
@article{389ad7c8-6d1b-4094-98d3-94e153241d71,
  abstract     = {In this study, we sought to determine the effect of the quantitative trait locus Pia7 on arthritis severity. The regulatory locus derived from the arthritis-resistant E3 rat strain was introgressed into the arthritis-susceptibility DA strain through continuous backcrossing. Congenic rats were studied for their susceptibility to experimental arthritis using pristane and adjuvant oil. In addition, cell number and function of various leukocyte populations were analyzed either under naive or stimulated conditions. We found that the minimal congenic fragment of DA.E3-Pia7 rats overlapped with the minimal fragment in DA.PVG-Oia2 congenic rats, which has been positionally cloned to the antigen-presenting lectin-like receptor complex (APLEC) genes. DA.E3-Pia7 congenic rats were protected from both PIA and OIA, but the protection was more pronounced in OIA. In adoptive transfer experiments we observed that the Pia7 locus controlled the priming of arthritogenic T cells and not the effector phase. In addition, Pia7 congenic rats had a significant higher frequency of B cells and granulocytes as well as TNFalpha production after stimulation, indicating a higher activation state of cells of the innate immune system. In conclusion, this study shows that the APLEC locus is a major locus regulating the severity of experimentally induced arthritis in rats.Genes and Immunity advance online publication, 4 March 2010; doi:10.1038/gene.2010.2.},
  author       = {Rintisch, Carola and Kelkka, T and Norin, U and Lorentzen, J C and Olofsson, P and Holmdahl, Rikard},
  issn         = {1476-5470},
  language     = {eng},
  pages        = {239--245},
  publisher    = {Nature Publishing Group},
  series       = {Genes and Immunity},
  title        = {Finemapping of the arthritis QTL Pia7 reveals co-localization with Oia2 and the APLEC locus.},
  url          = {http://dx.doi.org/10.1038/gene.2010.2},
  volume       = {Apr 7},
  year         = {2010},
}