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Stefan Magez

Prof. Dr. ir. Stefan MAGEZ



​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. congolenseT. vivaxT. brucei and T. evansi).
With respect to the development of new diagnostic tools and treatment modalities, we have adopted the Nanobody® technology. 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.


Room E8.01
Vrije Universiteit Brussel
Pleinlaan 2
1050 Brussels


Tipping the balance between erythroid cell differentiation and induction of anemia in response to the inflammatory pathology associated with chronic trypanosome infections


Front Immunol. 2022 Nov 7;13:1051647. doi: 10.3389/fimmu.2022.1051647. eCollection 2022.


PMID: 36420267 | PMC: PMC9676970 | DOI: 10.3389/fimmu.2022.1051647

Recent progress in diagnosis and treatment of Human African Trypanosomiasis has made the elimination of this disease a realistic target by 2030


Front Med (Lausanne). 2022 Nov 3;9:1037094. doi: 10.3389/fmed.2022.1037094. eCollection 2022.


PMID: 36405602 | PMC: PMC9669443 | DOI: 10.3389/fmed.2022.1037094

The Pathogenesis of African Trypanosomiasis


Annu Rev Pathol. 2022 Sep 2. doi: 10.1146/annurev-pathmechdis-031621-025153. Online ahead of print.


PMID: 36055769 | DOI: 10.1146/annurev-pathmechdis-031621-025153

The Role of MIF and IL-10 as Molecular Yin-Yang in the Modulation of the Host Immune Microenvironment During Infections: African Trypanosome Infections as a Paradigm


Front Immunol. 2022 Apr 7;13:865395. doi: 10.3389/fimmu.2022.865395. eCollection 2022.


PMID: 35464430 | PMC: PMC9022210 | DOI: 10.3389/fimmu.2022.865395

Detrimental Effect of Trypanosoma brucei brucei Infection on Memory B Cells and Host Ability to Recall Protective B-cell Responses


J Infect Dis. 2022 Aug 26;226(3):528-540. doi: 10.1093/infdis/jiac112.


PMID: 35363871 | DOI: 10.1093/infdis/jiac112