In high-transmission areas, individuals show increased proportions of CD4+FOXP3+CD127lo/− Tregs with an effector memory phenotype that suppress malaria antigen-induced cytokine production, maintaining immune homeostasis.294 Acute infections with P. vivax and P. falciparum induce expanded Treg populations and altered dendritic cell ratios, correlating with parasite load but not clinical severity.295 Increased Treg numbers are also associated with lethal P. berghei and P. yoelii infections.296. The gene discussed is CD4; the disease is malaria.