PMID- 16160826
OWN - NLM
STAT- MEDLINE
DCOM- 20060112
LR  - 20181113
IS  - 0093-7711 (Print)
IS  - 0093-7711 (Linking)
VI  - 57
IP  - 9
DP  - 2005 Oct
TI  - Polymorphism of the mouse gene for the interleukin 10 receptor alpha chain 
      (Il10ra) and its association with the autoimmune phenotype.
PG  - 697-702
AB  - Several studies suggest that interleukin (IL)-10 pathway is involved in murine 
      lupus, while no linkage of IL-10 gene polymorphism to disease susceptibility has 
      been reported in studies with lupus-prone mice. Since IL-10 functions through the 
      specific IL-10 receptor alpha (IL-10RA) chain and the IL-10RA gene (Il10ra) is 
      linked to the susceptibility loci of atopic dermatitis and Crohn's disease 
      identified using mouse models, we supposed that IL-10RA might be involved in 
      murine lupus. By flow cytometry analysis, we found that NZW mice, one of the 
      parental strains of lupus-prone (NZBxNZW) F1 mice, express extremely low levels 
      of IL-10RA compared with NZB mice, the other parental strain, and the healthy 
      BALB/c and C57BL/6 mice. Sequence analyses of Il10ra cDNA of NZW mice showed 
      multiple nucleotide mutations compared with that of NZB and C57BL/6 strains, some 
      of which would result in amino acid substitutions in the IL-10RA protein. 
      Lupus-prone MRL mice shared the same polymorphism with NZW. Analyses using 
      (NZBxNZW) F1xNZB backcross mice showed that high serum levels of IgG 
      antichromatin antibodies were regulated by a combinatorial effect of the NZW 
      Il10ra allele and a heterozygous genotype for Tnfa microsatellite locus. Our data 
      suggest that the polymorphic NZW-type Il10ra may be involved in the pathologic 
      production of antichromatin antibodies and, if so, may contribute in part to the 
      development of systemic lupus erythematosus as one susceptibility allele.
FAU - Qi, Zan-Mei
AU  - Qi ZM
AD  - Central Laboratory, the First Affiliated Hospital, China Medical University, 155 
      Nan-Jing Bei, Shenyang, Liaoning, 110001, PR China.
FAU - Wang, Jun
AU  - Wang J
FAU - Sun, Zheng-Rong
AU  - Sun ZR
FAU - Ma, Feng-Mao
AU  - Ma FM
FAU - Zhang, Qing-Rui
AU  - Zhang QR
FAU - Hirose, Sachiko
AU  - Hirose S
FAU - Jiang, Yi
AU  - Jiang Y
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20051018
PL  - United States
TA  - Immunogenetics
JT  - Immunogenetics
JID - 0420404
RN  - 0 (DNA Primers)
RN  - 0 (Protein Subunits)
RN  - 0 (Receptors, Interleukin)
RN  - 0 (Receptors, Interleukin-10)
SB  - IM
MH  - Animals
MH  - Crosses, Genetic
MH  - DNA Primers
MH  - *Genetic Predisposition to Disease
MH  - Lupus Erythematosus, Systemic/*genetics/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred MRL lpr
MH  - Mice, Inbred NZB
MH  - Phenotype
MH  - *Polymorphism, Genetic
MH  - Protein Subunits/genetics
MH  - Receptors, Interleukin/biosynthesis/*genetics
MH  - Receptors, Interleukin-10
MH  - Species Specificity
EDAT- 2005/09/15 09:00
MHDA- 2006/01/13 09:00
CRDT- 2005/09/15 09:00
PHST- 2005/03/28 00:00 [received]
PHST- 2005/07/27 00:00 [accepted]
PHST- 2005/09/15 09:00 [pubmed]
PHST- 2006/01/13 09:00 [medline]
PHST- 2005/09/15 09:00 [entrez]
AID - 10.1007/s00251-005-0036-7 [doi]
PST - ppublish
SO  - Immunogenetics. 2005 Oct;57(9):697-702. doi: 10.1007/s00251-005-0036-7. Epub 2005 
      Oct 18.