With respect to cellular immune response, cardiac valves from patients with RHD show an intense inflammatory infiltrate of mononuclear cells. These cells are able to produce cytokines and soluble mediators that affect valvular interstitial cell and valvular endothelial cell functions49,50. CD4+ T lymphocytes are highly reactive against cardiac myosin epitopes in RHD51-54. Proinflammatory cytokines, such as TNF-α, IFN-γ, IL-1, and IL-17, have been shown to be associated with diseaseprogression55, 56. IL-10, a modulatory cytokine, is present at high levels in patients with RHD and has a direct correlation with the CD8+ T lymphocyte response57-59. Macrophages are abundant in valvular inflammatory infiltrate and play an important role in production of both cytokine and matrix metalloproteinases, thus interfering in the remodeling of extracellular matrix components and fibrosis