DESCRIPTION:

QTL associated with cyclophosphamide induced apoptosis. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (66992757)

LABEL:

QTL-Capop-Mouse-Chr 1

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2020-05-06

SPECIES:

URI:

http://www.informatics.jax.org/searches/accession_report.cgi?id=MGI:1890950

AUTHORS:

Bergman ML, Cilio CM, Penha-Gonalves C, Lamhamedi-Cherradi SE, Lfgren A, Colucci F, Lejon K, Garchon HJ, Holmberg D

TITLE:

CTLA-4-/- mice display T cell-apoptosis resistance resembling that ascribed to autoimmune-prone non-obese diabetic (NOD) mice.

JOURNAL:

Journal of autoimmunity Mar 2001, Vol 16, pp. 105-13

ABSTRACT:

The genes conferring susceptibility to autoimmune (insulin-dependent) diabetes mellitus (IDDM) are, in most cases, not defined. Among the loci so far identified as associated with murine IDDM (Idd1-19), only the nature of Idd1 has been assessed. Here we show that thymocytes and peripheral lymphocytes of the non-obese diabetic (NOD) mouse are relatively resistant to apoptosis induced by gamma-irradiation. By linkage analysis of F2 progeny mice, we map this trait to a locus on chromosome 1 containing the Idd5 diabetes susceptibility region. By the use of congenic mice, we confirm the linkage data and map this locus to a 6 cM region on proximal chromosome 1. Ctla4, being localized in this chromosomal region and mediating crucial functions in T cell biology, is a logical candidate gene in the Idd5 susceptibility region. In line with this, we demonstrate that T cells from Ctla4(-/-)deficient mice show a similar resistance to gamma-irradiation-induced apoptosis as observed in the NOD mice. This reinforces the notion that CTLA-4 contributes to the pathogenesis of autoimmune diabetes. PUBMED: 11247636
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