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Sci. STKE, 19 July 2005
Vol. 2005, Issue 293, p. pe36
[DOI: 10.1126/stke.2932005pe36]

PERSPECTIVES

Host Cell Signaling and Trypanosoma cruzi Invasion: Do All Roads Lead to Lysosomes?

Barbara A. Burleigh*

Department of Immunology and Infectious Diseases, Harvard School of Public Health, 665 Huntington Avenue, Building I, Room 817, Boston, MA 02115, USA.

Summary: Trypanosoma cruzi, the protozoan parasite that causes Chagas’ disease in humans, is capable of invading and replicating within a wide variety of nucleated mammalian cell types. Host cell invasion by infective T. cruzi trypomastigotes is governed by parasite-triggered activation of host cell signaling pathways. Recent studies highlighting a role for host cell phosphatidylinositol 3-kinases (PI3Ks) in the T. cruzi invasion process have revealed surprising new insights into the mechanism of host cell invasion by this pathogen. In this Perspective, we discuss these findings and propose alternative models of T. cruzi invasion that incorporate this new information.

*Corresponding author. E-mail: bburleig{at}hsph.harvard.edu

Citation: B. A. Burleigh, Host Cell Signaling and Trypanosoma cruzi Invasion: Do All Roads Lead to Lysosomes? Sci. STKE 2005, pe36 (2005).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
A Novel IFN Regulatory Factor 3-Dependent Pathway Activated by Trypanosomes Triggers IFN-{beta} in Macrophages and Fibroblasts.
A.-D. C. Chessler, L. R. P. Ferreira, T.-H. Chang, K. A. Fitzgerald, and B. A. Burleigh (2008)
J. Immunol. 181, 7917-7924
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Human Autoantibodies Specific for Neurotrophin Receptors TrkA, TrkB, and TrkC Protect against Lethal Trypanosoma cruzi Infection in Mice.
B. Lu, J. Alroy, A. O. Luquetti, and M. PereiraPerrin (2008)
Am. J. Pathol. 173, 1406-1414
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Signaling During Pathogen Infection.
S. Munter, M. Way, and F. Frischknecht (2006)
Sci. STKE 2006, re5
   Abstract »    Full Text »    PDF »

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