About the Cover
COVER PICTURE: Malaria parasites multiply in the liver and then undergo several rounds of replication in erythrocytes. Here, variant antigens mediate adhesion of infected erythrocytes to ligands on host cells including myeloid dendritic cells and macrophages. Immune responses against the malaria parasites include both CD4+ and CD8+ cytotoxic T cells that can recognize intra-hepatic parasites, antibodies inhibiting invasion of erythrocytes, antibodies recognizing the adhesive, variant proteins on the surface of erythrocytes, phagocytosis by splenic macrophages, and antibody-dependent cytotoxicity. It now appears that at least two species of malaria parasites may subvert immune responses mediated directly or indirectly by myeloid cells during the blood stage of infection. In this issue, Ocana-Morgner et al.
(pages 143-151)
and the accompanying Commentary by Urban and Roberts
(pages 137-141)
describe inhibition of CD81 T cell responses during murine malaria infection (A). Other workers have shown inhibition of myeloid dendritic cell (B) and of macrophage function (C) mediated by the adhesion of falciparum-infected erythrocytes to CD36 and/or CD51. (Illustration by Mrs. Gerry Black.)
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