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Leishmania infection: surfaces and immunity
1Department of International Education, Royal Tropical Institute, Amsterdam, The Netherlands.
Abstract:
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.
Insights
Leishmania parasites infect macrophages using surface molecules like gp63 and lipophosphoglycan for cell entry and survival. Understanding these interactions is key to fighting leishmaniasis infections.
Area of Science:
- Parasitology
- Immunology
- Cell Biology
Background:
- Leishmania infections begin with sandfly bites, introducing parasites that invade macrophages.
- The mechanisms of parasite entry and intracellular survival remain incompletely understood.
- Parasite surface molecules are crucial for host cell interaction and infectivity.
Purpose of the Study:
- To elucidate the roles of Leishmania surface molecules in macrophage invasion and intracellular survival.
- To discuss the interactions between parasite surface components and macrophage receptors.
- To briefly describe immune responses relevant to leishmaniasis diagnosis and control.
Main Methods:
- Analysis of Leishmania surface molecules, including promastigote surface protease (gp63) and lipophosphoglycan.
- Discussion of molecular interactions with macrophage receptors (mannose, fucose, complement).
- Review of immune responses in infected humans and experimental animals.
Main Results:
- gp63 facilitates macrophage binding via mannose, fucose, and complement receptors.
- Lipophosphoglycan activates complement, aiding parasite attachment to macrophages.
- Other surface structures (acid phosphatase, glycolipids, membrane proteins) may aid attachment and intracellular survival by inhibiting host enzymes.
Conclusions:
- Leishmania surface molecules are critical for both initial host cell invasion and subsequent intracellular persistence.
- Understanding these molecular interactions provides insights into parasite pathogenesis.
- Immune responses to parasite antigens are important for protection, diagnosis, and epidemiology of leishmaniasis.