The malaria parasite Plasmodium falciparum is one of the most successful hu
man pathogens. Specific virulence factors remain poorly defined, although t
he adhesion of infected erythrocytes to the venular endothelium has been as
sociated with some of the syndromes of severe disease(1). Immune responses
cannot prevent the development of symptomatic infections throughout life, a
nd clinical immunity to the disease develops only slowly during childhood.
An understanding of the obstacles to the development of protective immunity
is crucial for developing rational approaches to prevent the disease. Here
we show that intact malaria-infected erythrocytes adhere to dendritic cell
s, inhibit the maturation of dendritic cells and subsequently reduce their
capacity to stimulate T cells. These data demonstrate both a novel mechanis
m by which malaria parasites induce immune dysregulation and a functional r
ole beyond endothelial adhesion for the adhesive phenotypes expressed at th
e surface of infected erythrocytes.