Abstract
In this article, we discuss an alternative explanation for the fact that the production and plasma levels of IL-17 are diminished in patients chronically infected with Trypanosoma cruzi, suffering from congestive heart failure. This alternate hypothesis considers the inhibitory pharmacological action of digoxin, a drug commonly used to treat heart failure. We believe this is a significant point to be further studied as IL-17 was initially considered to be heart-protective. Therefore, our argument has profound therapeutic implications
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