| First Author | Grässl G | Year | 1997 |
| Journal | Circulation | Volume | 95 |
| Issue | 7 | Pages | 1773-6 |
| PubMed ID | 9107162 | Mgi Jnum | J:40082 |
| Mgi Id | MGI:87421 | Doi | 10.1161/01.cir.95.7.1773 |
| Citation | Grassl G, et al. (1997) Induction of autoimmune myocarditis in interleukin-2-deficient mice. Circulation 95(7):1773-6 |
| abstractText | BACKGROUND: Interleukin (IL)-2 is an important growth and survival factor for T cells and plays a crucial role in inflammation. Myosin-induced myocarditis is strictly dependent on activated T cells and is a model for postinfectious inflammatory heart disease in humans. To explore the role of IL-2 in myocarditis, we injected mice genetically deficient for IL-2 with cardiac myosin. Because it is conceivable that the lack of IL-2 either promotes or ameliorates the disease, we selected mouse strains that differ in their susceptibility to cardiac myosin-induced myocarditis. METHODS AND RESULTS: Mice from a susceptible strain (C3H) that were rendered IL-2 deficient by gene targeting (IL-2-/- mice) and littermate controls were immunized twice with purified cardiac myosin at a 7-day interval. Three weeks after the first immunization, hearts were obtained for histopathological and immunohistochemical analysis. Sera were tested for autoantibodies to the cardiac myosin isoform by enzyme-linked immunosorbent assay. The majority of C3H IL-2-/- mice developed severe myocarditis accompanied by high-titer myosin autoantibodies. In C57BL/6 mice, which develop only little myocarditis on myosin immunization, lack of IL-2 did not increase susceptibility to the disease. Moreover, the composition of the inflammatory infiltrate in C3H IL-2-/- mice was virtually identical to that seen in the wild-type strain. CONCLUSIONS: Our data provide the first genetic evidence that in cardiac myosin-immunized mice, IL-2 has no essential role for the development of autoimmune heart disease and the generation of myosin autoantibodies. |
