This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jones, T. C. Search for Related Content PubMed PubMed Citation Articles by Jones, T. C.

American Journal of Pathology, Vol 102, 127-132, Copyright © 1981 by American Society for Investigative Pathology

REGULAR ARTICLES

Interactions between murine macrophages and obligate intracellular protozoa

TC Jones

The diversity of interactions between obligate intracellular protozoa and murine macrophages is just being elucidated. Protozoa of the genera Toxoplasma, Leishmania, and Trypanosoma all enter and replicate within macrophages. This review describes similarities and differences among these organisms with regard to entry mechanisms, sites of replication in the phagolysosomal system, metabolic requirements, effects on macrophage function, macrophage handling of protozoal antigens, the relationship to genetics of immune response, and the characteristics of lymphokine-induced microbicidal and microbistatic processes. These organisms each enter the macrophage by endocytosis, but they then reside at different sites in relation to the phagolysosomal system. The basis of obligate parasitism remains unknown; however, both the protozoa and the host cell have important effects on the function of the other during parasitism. The macrophage may play a pivotal role in the immunosuppression associated with the early stages of infection by each of these microbes. Genetic influences on the response to infection have been clearly identified in murine models. Lymphocyte products from immune cells have marked effects on the interactions of protozoa and macrophages, under some conditions stimulating protozoacidal mechanisms, and in some protozoastatic responses. The dynamic balance between protozoal parasitism and macrophage response must be further defined in order to determine the potential value of chemotherapeutic or immunologic intervention.

This article has been cited by other articles:

				S. Wei, F. Marches, J. Borvak, W. Zou, J. Channon, M. White, J. Radke, M.-F. Cesbron-Delauw, and T. J. Curiel Toxoplasma gondii-Infected Human Myeloid Dendritic Cells Induce T-Lymphocyte Dysfunction and Contact-Dependent Apoptosis Infect. Immun., April 1, 2002; 70(4): 1750 - 1760. [Abstract] [Full Text] [PDF]