title: Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease in mice deficiency of IL-1RA.
abstract: The mouse strain BALB/c deficient in IL-1 receptor antagonist protein (Il-1ra) develops spontaneous arthritis disease (SAD) while the strain DBA/1 IL1rn (-/-) with the same deficiency does not. Previously, we mapped a QTL on chromosome 1 for SAD and then developed a congenic mouse strain BALB.D1-1(-/-) that contains the QTL genomic fragment associated with resistance from DBA/1(-/-) on a BALB/c(-/-) background. The congenic strain was relatively resistant to spontaneous arthritis and had delayed onset and reduced severity of disease. We obtained whole genome expression profiles from the spleen of the congenic strain BALB.D1-1(-/-) and four other strains, the wild type BALB/c, DBA/1 and the deficient DBA/1 IL1rn (-/-) and the BALB/c IL1rn (-/-). We then compared the similarities and differences between the congenic strain and the four parental strains. Here we report the selected potential causal genes based on differential expression levels as well as function of genes.
  
  
  
  There is a considerable number of genes that are differentially expressed between the congenic strain and the three parental strains, BALB/c, DBA/1, and DBA/1(-/-). However there only a few differentially expressed genes were identified by comparing the congenic strain and the BALB/c(-/-)strain. These differentially expressed genes are mainly from T-cell receptor beta chain (Tcrb) and interferon-activatable protein (Ifi) genes. These genes are also differentially expressed between congenic strain and BALB/c strains. However, their expression levels in the congenic strain are similar to that in DBA/1 and DBA/1(-/-). The expression level of Tcrb-j gene is positively associated with two genes of Ifi gene 200 cluster.
  
  
  
  Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease and with down regulation of expressions of Tcrb genes in the mouse congenic strain. Ifi genes may play an important role in the susceptibility to SAD in mice.
authors.affiliation: Mudanjiang Medical College, Mudanjiang, HeilongJiang, 157001, People's Republic of China.|Department of Orthopaedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center (UTHSC), Memphis, TN, 38163, USA.
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Liu
authors.affiliation: Mudanjiang Medical College, Mudanjiang, HeilongJiang, 157001, People's Republic of China. yjiao2@uthsc.edu.|Department of Orthopaedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center (UTHSC), Memphis, TN, 38163, USA. yjiao2@uthsc.edu.
authors.forename: Yan
authors.initials: Y
authors.lastname: Jiao
authors.affiliation: Department of Orthopaedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center (UTHSC), Memphis, TN, 38163, USA.|Institute of Kaschin-beck Disease, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, 150081, China.|Key Laboratory of Etiologic Epidemiology, Education Bureau of Heilongjiang Province & Ministry of Health (23618104), Harbin, 150081, China.
authors.forename: Yanhong
authors.initials: Y
authors.lastname: Cao
authors.affiliation: Department of Medicine, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
authors.forename: Nan
authors.initials: N
authors.lastname: Deng
authors.affiliation: Department of Orthopaedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center (UTHSC), Memphis, TN, 38163, USA.
authors.forename: Yonghui
authors.initials: Y
authors.lastname: Ma
authors.affiliation: Department of Orthopaedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center (UTHSC), Memphis, TN, 38163, USA.|Research Service, Veterans Affairs Medical Center, 1030 Jefferson Avenue, Memphis, TN, 38104, USA.
authors.forename: Karen A
authors.initials: KA
authors.lastname: Hasty
authors.affiliation: Department of Medicine, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
authors.forename: Andrew
authors.initials: A
authors.lastname: Kang
authors.affiliation: Center of integrative research, The first Hospital of Qiqihaer City, 30 Gongyuan Road, Longsha District, Qiqihaer, Heilongjiang, 161005, People's Republic of China.
authors.forename: Hong
authors.initials: H
authors.lastname: Chen
authors.affiliation: Department of Medicine, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.|Research Service, Veterans Affairs Medical Center, 1030 Jefferson Avenue, Memphis, TN, 38104, USA.
authors.forename: John M
authors.initials: JM
authors.lastname: Stuart
authors.affiliation: Department of Orthopaedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center (UTHSC), Memphis, TN, 38163, USA. wgu@uthsc.edu.|Research Service, Veterans Affairs Medical Center, 1030 Jefferson Avenue, Memphis, TN, 38104, USA. wgu@uthsc.edu.
authors.forename: Weikuan
authors.initials: W
authors.lastname: Gu
mesh_terms: D000818:Animals; D001168:Arthritis / Q000235:genetics*; D003198:Computer Simulation; D005260:Female; D020869:Gene Expression Profiling; D019674:Genes, T-Cell Receptor beta / Q000235:genetics*; D000068617:Genetic Background; D053590:Interleukin 1 Receptor Antagonist Protein / Q000235:genetics*; D051379:Mice; D020297:Mice, Congenic; D008807:Mice, Inbred BALB C; D008811:Mice, Inbred DBA; D008817:Mice, Mutant Strains; D046228:Microarray Analysis; D009154:Mutation / Q000235:genetics; D009687:Nuclear Proteins / Q000235:genetics*; D010641:Phenotype; D013045:Species Specificity
chemical_list: C484444:HIN-200 protein, mouse; D053590:Interleukin 1 Receptor Antagonist Protein; D009687:Nuclear Proteins