DESCRIPTION:

QTL associated with anticardiolipin antibody 2. The confidence interval is Chr4:94736033-28006254 bp,+strand

LABEL:

QTL-Acla2-Mouse-Chr 4

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2024-04-25

SPECIES:

URI:

http://www.informatics.jax.org/searches/accession_report.cgi?id=MGI:3625040

AUTHORS:

Ida A, Hirose S, Hamano Y, Kodera S, Jiang Y, Abe M, Zhang D, Nishimura H, Shirai T

TITLE:

Multigenic control of lupus-associated antiphospholipid syndrome in a model of (NZW x BXSB) F1 mice.

JOURNAL:

European journal of immunology Sep 1998, Vol 28, pp. 2694-703

ABSTRACT:

In a subset of systemic lupus erythematosus (SLE) patients, antiphospholipid syndrome, characterized by occurrence of anti-cardiolipin (CL) antibodies, thrombocytopenia, thrombosis and recurrent intrauterine fetal death occurs. Male (NZW x BXSB)F1 mice, carrying the BXSB Yaa gene, serve as a model for SLE-associated antiphospholipid syndrome. Using microsatellite markers in the NZW x (NZW x BXSB)F1 backcross male progeny, we mapped BXSB alleles contributing to the generation of anti-CL antibodies, platelet-binding antibodies, thrombocytopenia and myocardial infarction. Generation of each disease character was controlled by two major independently segregating dominant alleles, i.e. those on chromosomes (Chr.) 4 and 17 for anti-CL antibodies, Chr. 8 and 17 for both anti-platelet antibodies and thrombocytopenia and, to our surprise, Chr. 7 and 14 for myocardial infarction, and that a combination of the two alleles appeared to produce full expression of each character, as a complementary gene action. The alleles on Chr. 17 linked to the above three characters were all mapped in close proximity to the H-2 complex. Therefore, no single factor such as anti-CL antibodies can explain the pathogenesis of SLE-associated antiphospholipid syndrome. Rather, a combination of susceptibility alleles such as described here, along with additional modifying loci, i.e. BXSB Yaa and some from NZW, characterizes unique SLE features in male (NZW x BXSB) F1 mice. There are potentially important candidate genes which may be linked to the syndrome. PUBMED: 9754557
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