Publications by authors named "H Pietrzak"
Article Synopsis
- Asymptomatic infections of P. falciparum malaria in adults may hinder clinical immunity rather than support it, serving as a reservoir for the parasite and aiding its transmission.
- Researchers used a systems approach involving antibody responses and cell profiling to study the immune responses in individuals with symptomatic and asymptomatic malaria, linking certain immune cell profiles to a lower risk of clinical malaria.
- Findings indicate that while some immune responses exist, asymptomatic infections also promote immunosuppressive mechanisms that could undermine effective immune control and vaccine responsiveness against malaria.
Article Synopsis
- The study explores the complex role of IFN-γ in malaria, particularly its influence on T follicular helper cells and memory B cells, which are crucial for effective antibody responses and immunity.
- Through single-cell mass cytometry, distinct populations of CD4+ T cells with the T-bet factor were identified, showing varying risks for Plasmodium vivax malaria outcomes, indicating that inflammation can sometimes be beneficial.
- Additionally, specific types of memory B cells and T cell subsets were linked to reduced risk of symptomatic malaria, while others contributed to protection against asymptomatic infections, highlighting the need for both antibody and cell-mediated immunity in managing malaria.
Emerging evidence started to delineate multiple layers of memory B cells, with distinct effector functions during recall responses. Whereas most studies examining long-lived memory B cell responses have focussed on the IgG+ memory B cell compartment, IgM+ memory B cells have only recently started to receive attention. It has been proposed that unlike IgG+ memory B cells, which differentiate into antibody-secreting plasma cells upon antigen re-encounter, IgM+ memory B cells might have the additional capacity to establish secondary germinal centre (GC) responses.
View Article and Find Full Text PDFDespite the key role that antibodies play in protection, the cellular processes mediating the acquisition of humoral immunity against malaria are not fully understood. Using an infection model of severe malaria, we find that germinal center (GC) B cells upregulate the transcription factor T-bet during infection. Molecular and cellular analyses reveal that T-bet in B cells is required not only for IgG switching but also favors commitment of B cells to the dark zone of the GC.
View Article and Find Full Text PDFPlasmodium falciparum, which causes malaria, extensively remodels its human host cells, particularly erythrocytes. Remodelling is essential for parasite survival by helping to avoid host immunity and assisting in the uptake of plasma nutrients to fuel rapid growth. Host cell renovation is carried out by hundreds of parasite effector proteins that are exported into the erythrocyte across an enveloping parasitophorous vacuole membrane (PVM).
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