The tegumental surface membranes of Schistosoma mansoni are enriched in parasite-specific phospholipid species.

The complex surface structure of adult Schistosoma mansoni, the tegument, is essential for survival of the parasite. This tegument is syncytial and is covered by two closely-apposed lipid bilayers that form the interactive surface with the host. In order to identify parasite-specific phospholipids present in the tegument, the species compositions of the major glycerophospholipid classes, phosphatidylcholine, phosphatidylserine, phosphatidylethanolamine and phosphatidylinositol, including lysophospholipid species, were analysed in adult S.

Binding of von Willebrand factor and plasma proteins to the eggshell of Schistosoma mansoni.

Schistosoma mansoni eggs have to cross the endothelium and intestinal wall to leave the host and continue the life cycle. Mechanisms involved in this essential step are largely unknown. Here we describe direct binding to the S.

Schistosoma mansoni: the egg, biosynthesis of the shell and interaction with the host.

The schistosome eggshell is a hardened and tanned structure made from cross-linked proteins. It is synthesized within the female worm from many different kinds of proteins and glycoproteins. Once the egg is released in the circulation, the outer surface of the eggshell is exposed and hence a direct site of interaction between the parasite and the host.

The proteome of the insoluble Schistosoma mansoni eggshell skeleton.

In schistosomiasis, the majority of symptoms of the disease is caused by the eggs that are trapped in the liver. These eggs elicit an immune reaction that leads to the formation of granulomas. The eggshell, which is a rigid insoluble structure built from cross-linked proteins, is the site of direct interaction between the egg and the immune system.

Cutting edge: conventional dendritic cells are the critical APC required for the induction of experimental cerebral malaria.

Cerebral malaria (CM) is a serious complication of Plasmodium falciparum infection, causing significant morbidity and mortality among young children and nonimmune adults in the developing world. Although previous work on experimental CM has identified T cells as key mediators of pathology, the APCs and subsets therein required to initiate immunopathology remain unknown. In this study, we show that conventional dendritic cells but not plasmacytoid dendritic cells are required for the induction of malaria parasite-specific CD4+ T cell responses and subsequent experimental CM.