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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 109189, 13 pages
Review Article

Leishmania Interferes with Host Cell Signaling to Devise a Survival Strategy

Lab no. 5, National Center for Cell Science, University of Pune, Ganeshkhind, Pune 411 007, India

Received 31 July 2009; Revised 21 October 2009; Accepted 28 January 2010

Academic Editor: Abhay R. Satoskar

Copyright © 2010 Suvercha Bhardwaj et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The protozoan parasite Leishmania spp. exists as extracellular promastigotes in its vector whereas it resides and replicates as amastigotes within the macrophages of its mammalian host. As a survival strategy, Leishmania modulates macrophage functions directly or indirectly. The direct interference includes prevention of oxidative burst and the effector functions that lead to its elimination. The indirect effects include the antigen presentation and modulation of T cell functions in such a way that the effector T cells help the parasite survive by macrophage deactivation. Most of these direct and indirect effects are regulated by host cell receptor signaling that occurs through cycles of phosphorylation and dephosphorylation in cascades of kinases and phosphatases. This review highlights how Leishmania selectively manipulates the different signaling pathways to ensure its survival.