CMR FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Olivier, M.
Right arrow Articles by Forget, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Olivier, M.
Right arrow Articles by Forget, G.

 Previous Article  |  Next Article 

Clinical Microbiology Reviews, April 2005, p. 293-305, Vol. 18, No. 2
0893-8512/05/$08.00+0     doi:10.1128/CMR.18.2.293-305.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Subversion Mechanisms by Which Leishmania Parasites Can Escape the Host Immune Response: a Signaling Point of View

Martin Olivier,1,2,3* David J. Gregory,1,2 and Geneviève Forget4

Centre for the Study of Host Resistance at the Research Institute of the McGill University Health Centre,1 Department of Microbiology and Immunology,2 Department of Experimental Medicine, McGill University, Montréal,3 Centre de Recherche du CHUQ, Université Laval, Sainte-Foy, Québec, Canada4

The obligate intracellular parasite Leishmania must survive the antimicrobial activities of its host cell, the macrophage, and prevent activation of an effective immune response. In order to do this, it has developed numerous highly successful strategies for manipulating activities, including antigen presentation, nitric oxide and oxygen radical generation, and cytokine production. This is generally the result of interactions between Leishmania cell surface molecules, particularly gp63 and LPG, and less well identified macrophage surface receptors, causing the distortion of specific intracellular signaling cascades. We describe some of the signaling pathways and intermediates that are repressed in infected cells, including JAK/STAT, Ca2+-dependent protein kinase C (PKC) isoforms, and mitogen-activated protein kinases (especially ERK1/2), and proteasome-mediated transcription factor degradation. We also discuss protein tyrosine phosphatases (particularly SHP-1), intracellular Ca2+, Ca2+-independent PKC, ceramide, and the suppressors of cytokine signaling family of repressors, which are all reported to be activated following infection, and the role of parasite-secreted cysteine proteases.


* Corresponding author. Mailing address: McGill University, Department of Microbiology and Immunology, Duff Medical Building, Room 610, 3775 University St., Montréal, Québec H3A 2B4, Canada. Phone: (514) 398-5592/1302. Fax: (514) 398-7052. E-mail: martin.olivier{at}mcgill.ca.


Clinical Microbiology Reviews, April 2005, p. 293-305, Vol. 18, No. 2
0893-8512/05/$08.00+0     doi:10.1128/CMR.18.2.293-305.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Antimicrob. Agents Chemother. Clin. Vaccine Immunol.
J. Clin. Microbiol. ALL ASM JOURNALS

Copyright © 2005 by the American Society for Microbiology. All rights reserved.