TGFB1 and Plasmodium vivax malaria: Furthermore, in severe Plasmodium vivax malaria, high plasma heme raises SOD1 levels and lowers circulating TGF-β; adding heme to human peripheral blood mononuclear cells increases SOD1 secretion and activity while suppressing TGF-β release, and knocking down SOD1 restores TGF-β—consistent with SOD1-derived H2O2 mediating suppression; the effect was largely independent of CD14 (cluster of differentiation 14) [102].