Host Parasite Interactions and Evasion of Immune Responses
Our research focuses on understanding of various mechanisms underlying disfunction of the adaptive and the innate immune systems in response to salivarian trypanosomes. The latter are single celled extracellular parasites causing lethal infections in humans and animals. The interplay between the host and the parasite involves disabling protective B cells and T cells as well as reprogramming innate immune cells such as neutrophils. Our research group tries to understand different mechanisms and molecules involved in these processes occurring on the level of the bone marrow, the thymus, and secondary lymphoid organs. This, in turn, is expected to deliver new interventions strategies counteracting organ pathology.
Areas of Expertise
- B cell biology
- Vaccinology
- Host-parasite interactions
- Inflammation
- Transcriptomics
Technology Transfer Potential
- Identification of vaccine candidates and novel intervention strategies against parasitic diseases.
Selected publications
- Pham HTT, et al. Neutrophil metalloproteinase driven spleen damage hampers infection control of trypanosomiasis. Nat Commun. 14, 5418 (2023). Visit ➚
- Nguyen HTT, et al. Single-cell transcriptome profiling and the use of AID deficient mice reveal that B cell activation combined with antibody class switch recombination and somatic hypermutation do not benefit the control of experimental trypanosomosis. PLoS Pathog. 17(11):e1010026 (2021). Visit ➚
- Pays E, et al. The Pathogenesis of African Trypanosomiasis. Annu Rev Pathol. 18:19-45 (2023). Visit ➚
- Radwanska, M, et al. Macrophage-infectivity potentiator of Trypanosoma cruzi (TcMIP) is a new pro-type 1 immuno-stimulating protein for neonatal human cells and vaccines in mice. Front Immunol. 2023 Mar 23;14:1138526 (2023). Visit ➚
- Radwanska M, et al. Trypanosomiasis-induced B cell apoptosis results in loss of protective anti-parasite antibody responses and abolishment of vaccine-induced memory responses. PLoS Pathog. 4(5):e1000078 (2008). Visit ➚
Bibliography
- Full bibliography Visit ➚
The image represents immune responses in the spleen during early and chronic stages of a trypanosome infection. The early events led to rapid differentiation of mature B cells to IgG secreting plasma cells, in the presence of steadily increasing numbers of neutrophils. On the other hand, the chronic infection gives rise to depletion of mature B cells, lack of replenishment of the spleen by transitional B cells, and the presence of very high neutrophil numbers. The latter secrete high levels of metalloproteinases such as MMP-8 and MMP-9, responsible for remodeling of a spleen architecture. Image by Hang Nguyen and Magdalena Radwanska.