GeneSet Information

Tier II GS135311 • autoimmune ovarian dysgenesis 4 (Aod4, Published QTL Chr 2)

DESCRIPTION:

QTL associated with autoimmune ovarian dysgenesis 4. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (162212535)

LABEL:

QTL-Aod4-Mouse-Chr 2

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2019-01-07

SPECIES:

AUTHORS:

del Rio R, Sun Y, Alard P, Tung KS, Teuscher C

TITLE:

H2 control of natural T regulatory cell frequency in the lymph node correlates with susceptibility to day 3 thymectomy-induced autoimmune disease.

JOURNAL:

Journal of immunology (Baltimore, Md. : 1950) Jan 2011, Vol 186, pp. 382-9

ABSTRACT:

Day 3 thymectomy (D3Tx) results in a loss of peripheral tolerance mediated by natural regulatory T cells (nTregs) and development of autoimmune ovarian dysgenesis (AOD) and autoimmune dacryoadenitis (ADA) in A/J and (C57BL/6J × A/J) F(1) hybrids (B6A), but not in C57BL/6J (B6) mice. Previously, using quantitative trait locus (QTL) linkage analysis, we showed that D3Tx-AOD is controlled by five unlinked QTL (Aod1-Aod5) and H2. In this study, using D3Tx B6-Chr(A/J)/NaJ chromosome (Chr) substitution strains, we confirm that QTL on Chr16 (Aod1a/Aod1b), Chr3 (Aod2), Chr1 (Aod3), Chr2 (Aod4), Chr7 (Aod5), and Chr17 (H2) control D3Tx-AOD susceptibility. In addition, we also present data mapping QTL controlling D3Tx-ADA to Chr17 (Ada1/H2), Chr1 (Ada2), and Chr3 (Ada3). Importantly, B6-ChrX(A/J) mice were as resistant to D3Tx-AOD and D3Tx-ADA as B6 mice, thereby excluding Foxp3 as a susceptibility gene in these models. Moreover, we report quantitative differences in the frequency of nTregs in the lymph nodes (LNs), but not spleen or thymus, of AOD/ADA-resistant B6 and AOD/ADA-susceptible A/J, B6A, and B6-Chr17(A/J) mice. Similar results correlating with experimental allergic encephalomyelitis and orchitis susceptibility were seen with B10.S and SJL/J mice. Using H2-congenic mice, we show that the observed difference in frequency of LN nTregs is controlled by Ada1/H2. These data support the existence of an LN-specific, H2-controlled mechanism regulating the prevalence of nTregs in autoimmune disease susceptibility. PUBMED: 21135167
Find other GeneSets from this publication

Annotation Information



T-Lymphocytes (D013601)
Orchitis (D009920)
Prevalence (D015995)
Thymectomy (D013934)
Chromosomes (D002875)
Research Report (D058028)
Quantitative Trait Loci (D040641)
T-Lymphocytes, Regulatory (D050378)
Autoimmune Diseases (D001327)
Chimera (D002678)
Encephalomyelitis (D004679)
Disease Susceptibility (D004198)
Encephalomyelitis, Autoimmune, Experimental (D004681)
Dacryocystitis (D003607)
Lymph Nodes (D008198)
Thymus Gland (D013950)
lymph node (MA:0000139)
lacrimal gland inflammation (MP:0008880)
testis inflammation (MP:0001875)
CNS inflammation (MP:0006082)
chromosome (GO:0005694)

Gene List • 568 Genes

Uploaded As Gene Symbol Homology Score Priority LinkOuts Emphasis