Two Autoimmune Diabetes Loci Influencing T Cell Apoptosis Control Susceptibility to Experimental Autoimmune Myocarditis | Zendy

Mehmet Güler | Zendy; Davinna L. Ligons | Zendy; Yan Wang | Zendy; Michael J. Bianco | Zendy; Karl W. Broman | Zendy; Noel R. Rose | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Two Autoimmune Diabetes Loci Influencing T Cell Apoptosis Control Susceptibility to Experimental Autoimmune Myocarditis

Author(s) -

Mehmet Güler,

Davinna L. Ligons,

Yan Wang,

Michael J. Bianco,

Karl W. Broman,

Noel R. Rose

Publication year - 2005

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.174.4.2167

Subject(s) - immunology , immune system , biology , apoptosis , autoimmune disease , pathogenesis , nod mice , nod , autoimmunity , genetic predisposition , myocarditis , gene , genetics , medicine , antibody

The pathogenesis of immune-mediated myocarditis depends on genetic and environmental factors. To study the genetic mechanisms, we have developed a model of experimental autoimmune myocarditis in the A.SW mouse. Here we provide evidence that loci on murine chromosome 6, and possibly chromosome 1, are involved in regulating susceptibility. Moreover, these loci overlap with loci implicated in other autoimmune diseases including diabetes in the NOD mouse. These two loci also regulate apoptosis in thymocytes as well as peripheral T cells in the NOD mouse, and we report further that A.SW mice demonstrate the same characteristics in apoptosis. These results suggest that common pathogenetic mechanisms involving apoptosis of both thymic and peripheral T cells are shared by multiple autoimmune diseases.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research