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  • Title: Coxsackievirus B-3 myocarditis. T-cell autoimmunity to heart antigens is resistant to cyclosporin-A treatment.
    Author: Estrin M, Smith C, Huber S.
    Journal: Am J Pathol; 1986 Nov; 125(2):244-51. PubMed ID: 3024491.
    Abstract:
    A cardiotropic variant of coxsackievirus group B, Type 3 (CVB3) induces myocarditis in inbred Balb/c mice. Myocardial injury is predominantly mediated by T lymphocytes recognizing normal myocyte antigens, making this an autoimmune disease. Nonetheless, the autoimmune response cannot be inhibited by cyclosporin A (CSA) treatment of the infected animals. Mortality in treated mice was increased 2-4 times, but neither virus-specific antibody or cytolytic T-lymphocyte responses were affected, and maximal virus concentrations in the hearts of CSA-treated and control animals were similar. Cardiac damage remains T-cell-mediated, because mice given both CSA and rabbit anti-thymocyte serum (ATS) failed to develop significant myocardial inflammation. CSA did suppress immunity in Balb/c mice to an allogeneic C57B1 lymphoma, EL4. Subcutaneous inoculation of mice with 2.5 X 10(6) ascites tumor cells resulted in 100% of the CSA-treated animals having tumors averaging 340 mg 10 days later, compared with less than 10% of control animals having tumors averaging only 30 mg. Humoral immunity to the tumor was absent in CSA-treated mice. Therefore, whether CSA induces immunosuppression depends upon the antigenic stimulus used.
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