The focus of our research is to obtain a better insight into the mechanisms of infection-induced immunopathology during African trypanosomiasis, as well as to study pathways of parasitemia control. The ultimate goal of this research is the development of new diagnosis, vaccination and treatment strategies to control this parasitic disease, which currently affects both human and livestock in vast areas of sub-Saharan Africa. As model systems in our research, we use parasite strains that cause human sleeping sickness (T. rhodesiense and T. gambiense), as well as parasites that have a major economic impact by infecting livestock (T. congolense, T. vivax, T. brucei and T. evansi).
With respect to the development of new diagnostic tools and treatment modalities, we have adopted the Nanobody® technology (see Serge Muyldermans). While small antibody fragments such as Nanobodies® allow the targeting of unique surface epitopes on the parasite, their binding does not seem to be hindered by the presence of infection-associated conventional antibodies from the host. Hence, Nanobodies® are now being generated with the aim of (i) targeting trypanolytic drug compounds towards the parasite in a very specific manner, and (ii) developing new diagnostic tools that can recognize parasite antigens in the blood of infected patients.
At the level of immunopathology research, we mainly focus on analyzing the role of TNF in infection-associated anemia, as well as B-cell memory destruction. In the past, we have meticulously uncovered the role of the main parasite compounds involved in the induction of inflammatory TNF-mediated responses. Now, we are continuing this research in order to gain a better insight into actual trypanosomiasis disease development, as well as the role of inflammation in the destruction of vaccine-induced memory. The latter is crucial to understanding why all anti-trypanosome vaccination strategies appear to have failed so far.
In addition, structural biology investigations into the molecular interactions involved in cell invasion by parasites are performed.
- Adenylate cyclases of Trypanosoma brucei inhibit the innate immune response of the host Salmon D, Vanwalleghem G, Morias Y, Denoeud J, Krumbholz C, Lhommé F, Bachmaier S, Kador M, Gossmann J, Dias F, De Muylder G, Uzureau P, Magez S, Moser M, De Baetselier P, Van Den Abbeele J, Beschin A, Boshart M, Pays E. SCIENCE, 337, 463-6, 2012
- T. brucei Infection Reduces B Lymphopoiesis in Bone Marrow and Truncates Compensatory Splenic Lymphopoiesis through Transitional B-Cell Apoptosis Bockstal V, Guirnalda P, Caljon G, Goenka R, Telfer J, Frenkel D, Radwanska M, Magez S, Black S. PLoS Pathogens, 7, e1002089, 2011
- iNOS-producing inflammatory dendritic cells constitute the major infected cell type during the chronic Leishmania major infection phase of C57BL/6 resistant mice De Trez C, Magez S, Akira S, Ryffel B, Carlier Y, Muraille E. PLoS Pathogens, 5, e1000494, 2009
- Trypanosomiasis-induced B cell apoptosis results in loss of protective anti-parasite antibody responses and abolishment of vaccine-induced memory responses Radwanska M, Guirnalda P, De Trez C, Ryffel B, Black S, Magez S. PLoS Pathogens, 4, e1000078, 2008
- The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice Magez S, Schwegmann A, Atkinson R, Claes F, Drennan M, De Baetselier P, Brombacher F. PLoS Pathogens, 4, e1000122, 2008
All publications of Stefan Magez on Pubmed