Key result
Review highlights how genetics, molecular mimicry, and cytokines drive RHD pathogenesis and mitral valve damage.
This review summarizes the immunologic mechanisms, including molecular mimicry and cytokine responses, that drive the development of rheumatic mitral valve stenosis.
Informs research on immunologic drivers of rheumatic mitral stenosis; leaves open translation to targeted interventions.
Although the prevalence of rheumatic heart disease (RHD) has rapidly subsided over the last several decades in the United States, it still remains a serious cardiovascular disorder across the world, particularly in developing nations. Chronic autoimmune inflammation of the cardiac valves can result in mitral stenosis, increasing the risk of morbidity, mortality, and long-term sequelae in these patients. Researchers have begun to unravel the mysteries behind the development of RHD in the setting of chronic autoimmune inflammatory reactions and the roles genetic predisposition, antibody- and T-cell-mediated molecular mimicry, and cytokine proinflammatory responses play. In this article, the immunologic pathogenesis of RHD and its effects on the mitral valve are reviewed.
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Santana et al. (2011) conducted a review in Rheumatic heart disease and mitral stenosis. This review summarizes the immunologic pathogenesis of rheumatic heart disease and its effects on the mitral valve, highlighting genetic predisposition, molecular mimicry, and cytokine responses.
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