Leishmania infection: surfaces and immunity.
Infections with Leishmania parasites are initiated by bites from infected sandflies; the injected promastigotes are attacked by phagocytic cells but succeed in entering cells of the macrophage family and surviving in them. The secrets of the success of the extracellular form in penetrating the host cell and of the intracellular form in surviving in a potentially hostile environment are yet to be unraveled. The infectivity of the extracellular promastigote is related to the expression on its surface of molecules that interact with the surface of the host cell. One of these molecules is the promastigote surface protease, or gp63, which is also a dominant surface antigen; this enzyme is thought to be involved in binding to the macrophage via the cell receptors for mannose and fucose and for the third component of complement. Another important surface component is the lipophosphoglycan, consisting of a series of phosphorylated disaccharides linked to a novel lipid anchor in the membrane. This is also released from the parasite surface and was earlier identified as a highly immunogenic antigen excreted into culture medium. It can activate complement and may in this way promote attachment of the parasite to the macrophage. Other surface structures include the acid phosphatase, a glyco-inositol phospholipid, another glycolipid, and membrane proteins of 80 and 17 kilodaltons. All of these may play a role in attachment of the promastigote to the macrophage host cell, as well as in the survival of the amastigote within the macrophage, perhaps by inhibiting the activities of destructive enzymes. The roles in infectivity of these components of the Leishmania surfaces and their interactions with the various receptors on macrophages are discussed. The immune responses induced by these and other parasite antigens during infections in humans and experimental animals are also described briefly, especially those responses that may contribute to protection from infection, or to diagnosis and epidemiology.
Wright
E P
EP
Department of International Education, Royal Tropical Institute, Amsterdam, The Netherlands.
el Amin
E R
ER
D000818:Animals; D000953:Antigens, Protozoan / Q000502:physiology; D000954:Antigens, Surface / Q000502:physiology; D006790:Host-Parasite Interactions; D006801:Humans; D007891:Leishmania / Q000276:immunology / Q000502:physiology*; D007896:Leishmaniasis / Q000276:immunology* / Q000469:parasitology; D008264:Macrophages / Q000469:parasitology; D008563:Membrane Lipids / Q000502:physiology; D008565:Membrane Proteins / Q000502:physiology
D000953:Antigens, Protozoan; D000954:Antigens, Surface; D008563:Membrane Lipids; D008565:Membrane Proteins