| First Author | Eriksson U | Year | 2003 |
| Journal | Circulation | Volume | 107 |
| Issue | 2 | Pages | 320-5 |
| PubMed ID | 12538435 | Mgi Jnum | J:103083 |
| Mgi Id | MGI:3608441 | Doi | 10.1161/01.cir.0000043802.38699.66 |
| Citation | Eriksson U, et al. (2003) Interleukin-6-deficient mice resist development of autoimmune myocarditis associated with impaired upregulation of complement C3. Circulation 107(2):320-5 |
| abstractText | BACKGROUND: Interleukin (IL)-6 regulates various aspects of the immune response. In the context of heart diseases, it has been recognized as a prognostic factor for dilated cardiomyopathy, which often results from myocarditis. METHODS AND RESULTS: Using IL-6-deficient mice, we studied the role of IL-6 in a model of autoimmune myocarditis resulting from immunization with a peptide derived from cardiac alpha-myosin. Prevalence and severity of myocarditis were markedly reduced in the absence of IL-6. CD4+ T cells from immunized IL-6-deficient mice proliferated poorly on restimulation with specific antigen in vitro and did not mediate disease on adoptive transfer into IL-6-competent RAG-2-deficient mice, which otherwise lack B cells and T cells. Production of complement C3, a crucial factor for the development of myocarditis, was strongly upregulated in IL-6+/+ but not in IL-6-deficient mice after immunization. CONCLUSIONS: Our results demonstrate that IL-6 is required for the expansion of autoimmune CD4+ T cells and the pathogenesis of autoimmune myocarditis, possibly by upregulation of complement C3. |
