Abstract
Hypertension is the leading modifiable risk factor of worldwide morbidity and mortality because of its effects on cardiovascular and renal end-organ damage. Unfortunately, BP control is not sufficient to fully reduce the risks of hypertension, underscoring the need for novel therapies that address end-organ damage in hypertension. Over the past several decades, the link between immune activation and hypertension has been well established, but there are still no therapies for hypertension that specifically target the immune system. In this review, we describe the critical role played by T cells in hypertension and hypertensive end-organ damage and outline potential therapeutic targets to modulate T-cell phenotype and function in hypertension without causing global immunosuppression.