Unraveling the molecular signal pathways that govern parasite- induced B cell killing for the development of new immunological strategies in the fight against lymphoma diseases

Project Details


Our past research has provided clear evidence that trypanosomes have a profound negative effect on B cell homeostasis, can drive contact-dependent apoptosis of transitional B cells, abrogate B cell hybridoma cell proliferation upon cell-cell contact, and reduce the progression of multiple
myeloma plasmacytoma development. Our research hypothesis is that we can 'use' these parasite activities (not the parasite itself) in future intervention strategies in the fight against lymphoma diseases. These diseases comprise a group of white blood cell cancers, including B cell cancers. To reach our goal, clear insights need to be obtained into the molecular and cellular mechanisms that drive the B cell-killing activity of the parasite. The project has three major objectives: (i) Fully unravel the intracellular signaling pathways that are triggered during experimental trypanosome infections and drive FoB cell apoptosis, (ii) Track the effects of trypanosome B cell co-cultures
using the in vitro FoB-like A20 B cell lymphoma model, followed by in vivo assessment, and (iii) Identify the B cell surface molecules that serve as trypanosome recognition moieties able to trigger abrogation of B cells, and design a Nanobody-targeting strategy that can mimic the B cell killing effect of trypanosomes.
Effective start/end date1/01/1919/10/19

Flemish discipline codes

  • Applied immunology


  • Lymphoma