In
Plasmodium falciparum malaria, large proportions of resident macrophages and circulating monocytes and leukocytes contain massive amounts of the malarial pigment,
hemozoin. Previous studies have shown that important functions (e.g., the generation of the oxidative burst, the ability to repeat phagocytosis, and
protein kinase C activity) were severely impaired in
hemozoin-loaded monocytes. Expression of membrane
antigens directly involved in the immune response and in the phagocytic process, and/or under
protein kinase C control, in
hemozoin-loaded human monocytes was studied. Expression of major histocompatibility complex (MHC) class II after
gamma interferon stimulation was blocked in
hemozoin-loaded monocytes at the
protein expression and gene transcription levels but was preserved in control monocytes loaded with opsonized
latex beads or
anti-D(Rho)-
immunoglobulin G (
IgG)-opsonized human erythrocytes. Expression of CD54 (intracellular adhesion molecule 1) and CD11c (p150,95
integrin) was also decreased in
hemozoin-loaded monocytes. Expression of MHC class I, CD16 (low-affinity
Fc receptor for aggregated
IgG), CD32 (low-affinity
Fc receptor for aggregated
IgG), CD64 (high-affinity receptor for
IgG), CD11b (receptor for
complement component
iC3b [CR3]), CD35 (receptor for
complement components C3b and C4b [CR1]), and CD36 (non-class-A
scavenger receptor) was not specifically affected by
hemozoin loading. These results suggest that
hemozoin loading may contribute to the impairment of the immune response and the derangement of antigen presentation reported in previous studies of P.
falciparum malaria.