| First Author | Bergman ML | Year | 2001 |
| Journal | J Autoimmun | Volume | 16 |
| Issue | 2 | Pages | 105-13 |
| PubMed ID | 11247636 | Mgi Jnum | J:68151 |
| Mgi Id | MGI:1932191 | Doi | 10.1006/jaut.2000.0474 |
| Citation | Bergman ML, et al. (2001) CTLA-4-/- Mice Display T Cell-apoptosis Resistance Resembling that Ascribed to Autoimmune-prone Non-obese Diabetic (NOD) Mice. J Autoimmun 16(2):105-13 |
| abstractText | 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. Copyright 2001 Academic Press. |
