A locus on chromosome 1 promotes susceptibility of experimental autoimmune myocarditis and lymphocyte cell death

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....

Description complète

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 130(2009), 1 vom: 15. Jan., Seite 74-82
Auteur principal: Ligons, Davinna L (Auteur)
Autres auteurs: Guler, Mehmet L, Li, Haiyan S, Rose, Noel R
Format: Article en ligne
Langue:English
Publié: 2009
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, N.I.H., Extramural Caspases EC 3.4.22.- Myosins EC 3.6.4.1
Description
Résumé: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 lymphocytes 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
Description:Date Completed 14.01.2009
Date Revised 13.11.2018
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2008.06.015