Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease in mice deficiency of IL-1RA

Xiaoyun Liu, Yan Jiao, Yanhong Cao, Nan Deng, Yonghui Ma, Karen Hasty, Andrew Kang, Hong Chen, John Stuart, Weikuan Gu

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: 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. Results: 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. Conclusions: 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.

Original languageEnglish (US)
Article number25
JournalBMC Immunology
Volume17
Issue number1
DOIs
StatePublished - Aug 2 2016

Fingerprint

Arthritis
Genes
T-Cell Receptor beta Genes
Congenic Mice
T-Cell Receptor Genes
Interleukin-1 Receptors
Chromosomes, Human, Pair 1
Interferon-beta
Multigene Family
Proteins
Down-Regulation
Spleen
Genome

All Science Journal Classification (ASJC) codes

  • Immunology

Cite this

Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease in mice deficiency of IL-1RA. / Liu, Xiaoyun; Jiao, Yan; Cao, Yanhong; Deng, Nan; Ma, Yonghui; Hasty, Karen; Kang, Andrew; Chen, Hong; Stuart, John; Gu, Weikuan.

In: BMC Immunology, Vol. 17, No. 1, 25, 02.08.2016.

Research output: Contribution to journalArticle

@article{0f5beece0d964387911df9fc8939b5a0,
title = "Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease in mice deficiency of IL-1RA",
abstract = "Background: 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. Results: 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. Conclusions: 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.",
author = "Xiaoyun Liu and Yan Jiao and Yanhong Cao and Nan Deng and Yonghui Ma and Karen Hasty and Andrew Kang and Hong Chen and John Stuart and Weikuan Gu",
year = "2016",
month = "8",
day = "2",
doi = "10.1186/s12865-016-0163-y",
language = "English (US)",
volume = "17",
journal = "BMC Immunology",
issn = "1471-2172",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease in mice deficiency of IL-1RA

AU - Liu, Xiaoyun

AU - Jiao, Yan

AU - Cao, Yanhong

AU - Deng, Nan

AU - Ma, Yonghui

AU - Hasty, Karen

AU - Kang, Andrew

AU - Chen, Hong

AU - Stuart, John

AU - Gu, Weikuan

PY - 2016/8/2

Y1 - 2016/8/2

N2 - Background: 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. Results: 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. Conclusions: 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.

AB - Background: 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. Results: 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. Conclusions: 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.

UR - http://www.scopus.com/inward/record.url?scp=84980395660&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84980395660&partnerID=8YFLogxK

U2 - 10.1186/s12865-016-0163-y

DO - 10.1186/s12865-016-0163-y

M3 - Article

C2 - 27480124

AN - SCOPUS:84980395660

VL - 17

JO - BMC Immunology

JF - BMC Immunology

SN - 1471-2172

IS - 1

M1 - 25

ER -