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Targeting essential pathways in trypanosomatids gives insights into protozoan mechanisms of cell death

Despina Smirlis1*, Michael Duszenko2, Antonio Jiménez Ruiz3, Effie Scoulica4, Patrick Bastien5, Nicolas Fasel6 and Ketty Soteriadou1

Author Affiliations

1 Laboratory of Molecular Parasitology, Department of Microbiology, Hellenic Pasteur Institute, 127 Bas. Sofias Ave., 11521 Athens, Greece

2 Interfaculty Institute for Biochemistry (IFIB), University of Tübingen, Tübingen, Germany

3 Departamento de Bioquímica y Biología Molecular, Campus Universitario, Universidad de Alcalá, 28871 Alcalá de Henares, Madrid, Spain

4 Department of Clinical Bacteriology, Parasitology, Zoonoses and Geographical Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece

5 University Montpellier 1, UFR Médecine, Laboratoire de Parasitologie-Mycologie, 163 rue Auguste Broussonet, F-34090 Montpellier, France

6 Department of Biochemistry, 155 Chemin des Boveresses, University of Lausanne, Epalinges CH-1066, Switzerland

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Parasites & Vectors 2010, 3:107  doi:10.1186/1756-3305-3-107

Published: 17 November 2010


Apoptosis is a normal component of the development and health of multicellular organisms. However, apoptosis is now considered a prerogative of unicellular organisms, including the trypanosomatids of the genera Trypanosoma spp. and Leishmania spp., causative agents of some of the most important neglected human diseases. Trypanosomatids show typical hallmarks of apoptosis, although they lack some of the key molecules contributing to this process in metazoans, like caspase genes, Bcl-2 family genes and the TNF-related family of receptors. Despite the lack of these molecules, trypanosomatids appear to have the basic machinery to commit suicide. The components of the apoptotic execution machinery of these parasites are slowly coming into light, by targeting essential processes and pathways with different apoptogenic agents and inhibitors. This review will be confined to the events known to drive trypanosomatid parasites to apoptosis.