Chapter category: Infectious Disease

Avoidance of Innate Immune Mechanisms by the Protozoan Parasite, Leishmania spp.

This chapter appears in the following book:

Protozoans in Macrophages

Edited by: Eric Y. Denkers and Ricardo T. Gazzinelli
ISBN: 978-1-58706-150-9
» Get more information about this book at landesbioscience.com «

Chapter authors:
David M. Mosser and Suzanne A. Miles

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In this chapter, we will examine the mechanisms by which Leishmania parasites interact with host cells. We will try to develop the hypothesis that the success or failure of Leishmania infections can be traced to the initial mechanism(s) of parasite entry into mononuclear phagocytes. We will try to make the following points about the activation and modulation of innate immunity by Leishmania: First, promastigotes enter macrophages by a quiescent mechanism that fails to induce innate immune responses, and this may result in a delayed induction of an adaptive immune response. This delay in the development of adaptive immunity may provide the parasite with time to replicate within macrophages. Second, parasite replication disrupts macrophage responsiveness to the immune signals that are eventually generated. Third, the mechanism of amastigote entry into macrophages may also be the harbinger for successful parasitism. Amastigotes coat themselves in host IgG which ligates macrophage FcgR, resulting in the hyperproduction of IL-10 from infected macrophages. This IL-10 can prevent macrophage responses to IFN-g allowing the parasites to survive even in the immunologically intact host.

David M. Mosser
Department of Cell Biology and Molecular Genetics, University of Maryland

Suzanne A. Miles
Department of Cell Biology and Molecular Genetics, University of Maryland

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Chapter category: Infectious Disease

Avoidance of Innate Immune Mechanisms by the Protozoan Parasite, Leishmania spp.

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