ORCID Profile
0000-0002-4197-8393
Current Organisation
University of Oxford
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Publisher: Public Library of Science (PLoS)
Date: 07-2019
Publisher: American Society for Clinical Investigation
Date: 16-09-2019
DOI: 10.1172/JCI128865
Publisher: Public Library of Science (PLoS)
Date: 30-04-2008
Publisher: American Society for Clinical Investigation
Date: 04-2022
DOI: 10.1172/JCI157124
Publisher: The American Association of Immunologists
Date: 15-10-2001
DOI: 10.4049/JIMMUNOL.167.8.4729
Abstract: Natural immunity to malaria is characterized by low level CD4 T cell reactivity detected by either lymphoproliferation or IFN-γ secretion. Here we show a doubling in the detection rate of responders to the carboxyl terminus of circumsporozoite protein (CS) of Plasmodium falciparum by employing three T cell assays simultaneously: rapid IFN-γ secretion (ex vivo ELISPOT), IFN-γ secretion after reactivation of memory T cells and expansion in vitro (cultured ELISPOT), and lymphoproliferation. Remarkably, for no in idual peptide did a positive response for one T cell effector function correlate with any other. Thus these CS epitopes elicited unique T cell response patterns in malaria-exposed donors. Novel or important epitope responses may therefore be missed if only one T cell assay is employed. A borderline correlation was found between anti-CS Ab levels and proliferative responses, but no correlation was found with ex vivo or cultured IFN-γ responses. This suggested that the proliferating population, but not the IFN-γ-secreting cells, contained cells that provide help for Ab production. The data suggest that natural immunity to malaria is a complex function of T cell subgroups with different effector functions and has important implications for future studies of natural T cell immunity.
Publisher: Oxford University Press (OUP)
Date: 27-05-2010
DOI: 10.1093/HMG/DDQ216
Publisher: Springer Science and Business Media LLC
Date: 07-1999
DOI: 10.1038/21900
Abstract: The malaria parasite Plasmodium falciparum is one of the most successful human pathogens. Specific virulence factors remain poorly defined, although the adhesion of infected erythrocytes to the venular endothelium has been associated with some of the syndromes of severe disease. Immune responses cannot prevent the development of symptomatic infections throughout life, and clinical immunity to the disease develops only slowly during childhood. An understanding of the obstacles to the development of protective immunity is crucial for developing rational approaches to prevent the disease. Here we show that intact malaria-infected erythrocytes adhere to dendritic cells, inhibit the maturation of dendritic cells and subsequently reduce their capacity to stimulate T cells. These data demonstrate both a novel mechanism by which malaria parasites induce immune dysregulation and a functional role beyond endothelial adhesion for the adhesive phenotypes expressed at the surface of infected erythrocytes.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Britta Urban.