Key result
Coxsackievirus B3 infection transiently increases IK expression, which downregulates MHC class II expression on B cells through the induction of cAMP.
CVB3 infection downregulates MHC class II expression on B cells through IK-induced cAMP elevation, suggesting a mechanism of viral immune escape.
Major histocompatibility complex (MHC) class II expression is critical for the presentation of antigens in the immune response to viral infection. Consequently, some viruses regulate the MHC class II-mediated presentation of viral antigens as a mechanism of immune escape. In this study, we found that Coxsackievirus B3 (CVB3) infection transiently increased IK expression, which reduced the expression of MHC class II (I-A/I-E) on splenic B cells. Interestingly, CVB3-induced IK elevated cAMP, a downstream molecule of the G protein-coupled receptors, which inhibited MHC class II presentation on B cells. Transgenic mice expressing truncated IK showed lower expression of MHC class II on B cells than did wild-type mice after CVB3 infection. Taken together, these results imply that IK plays a role in downregulating MHC class II expression on B cells during CVB3 infection through the induction of cAMP.
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Park et al. (2013) studied Coxsackievirus B3 infection. Coxsackievirus B3 infection / Truncated IK expression vs. Wild-type mice was evaluated on MHC class II expression on B cells. Coxsackievirus B3 infection transiently increases IK expression, which downregulates MHC class II expression on B cells through the induction of cAMP.
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