Abstract
We previously identified by linkage analysis a region on chromosome 1 (Eam1) that confers susceptibility to experimental autoimmune myocarditis (EAM). To evaluate the role of Eam1, we created a congenic mouse strain, carrying the susceptible Eam1 locus of A.SW on the resistant B10.S background (B10.A-Eam1 congenic) and analyzed three outcomes: 1) the incidence and severity of EAM, 2) the susceptibility of lymph node cells (LNCs) to Cy-enhanced cell death, and 3) susceptibility of lymphoctyes to antigen-induced cell death. Incidence of myocarditis in B10.A-Eam1 congenic mice was comparable to A.SW mice, confirming that Eam1 plays an important role in disease development. Caspase 3, 8 and 9 activation in LNCs following Cy treatment and in CD4+ T cells after immunization with myosin/CFA was significantly lower in A.SW than B10.S mice whereas B10.A-Eam1 congenic mice exhibited an intermediate phenotype. Our results show that Eam1 reduces lymphocyte apoptosis and increases susceptibility to EAM.
Original language | English (US) |
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Pages (from-to) | 74-82 |
Number of pages | 9 |
Journal | Clinical Immunology |
Volume | 130 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2009 |
Externally published | Yes |
Keywords
- Apoptosis
- Autoimmune
- Caspase
- Chromosome
- Gene
- Locus
- Myocarditis
- Regulation
- Rodent
- Susceptibility
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology