Key Points
- To determine whether Coxsackievirus B3 infection and interferon gamma stimulation induce the expression of major histocompatibility complex antigens in cardiac myocytes.
- Induced acute viral myocarditis in C3H/He mouse ventricles using Coxsackievirus B3 (CVB3) and assessed MHC class I and II antigen expression via immunofluorescence.
- Treated cultured murine fetal cardiac myocytes in vitro with interferon gamma and evaluated MHC antigen expression using immunofluorescence and Northern blot hybridization with an antisense RNA probe.
- CVB3 infection provoked pronounced surface expression of the MHC class I H-2Kk product on cardiac myocytes, while MHC class II and H-2Dk products remained low or undetectable.
- Interferon gamma treatment of cultured myocytes induced high levels of MHC class I (H-2Kk) and weak-to-moderate MHC class II, confirming antigen upregulation is modulated at the transcriptional level.
- Capillary endothelial cells exhibited moderate, focal, and transient expression of both MHC class I (Kk and Dk) and MHC class II antigens between days 5 and 7 post-infection.
Structured PICO
Does Coxsackievirus B3 infection or interferon gamma treatment induce the expression of MHC antigens in murine cardiac myocytes?
PPopulationC3H/He mouse ventricles and cultured murine fetal cardiac myocytes
IInterventionCoxsackievirus B3 (CVB3) infection (in vivo) and interferon gamma treatment (in vitro)
CComparatorNormal cardiac myocytes
OOutcomeExpression of MHC class I and II antigenssurrogate
Coxsackievirus B3 infection and interferon gamma induce MHC class I antigen expression on murine cardiac myocytes, providing a mechanistic basis for T cell-mediated autoimmunity in viral myocarditis.