ArticleClinical and experimental immunology2002
Cytokine production and apoptosis among T cells from patients under treatment for Plasmodium falciparum malaria.
Article in Clinical and experimental immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 52 citations in OpenAlex.
- Changes in total and differential leukocyte counts during the clinically silent liver phase in a controlled human malaria infection in malaria-naïve Dutch volunteers.Malaria journal · 2017Trial
- Longevity and composition of cellular immune responses following experimental Plasmodium falciparum malaria infection in humans.PLoS pathogens · 2011Trial
- Evaluation of immunophenotypic alterations of peripheral blood lymphocytes and their sub-sets in uncomplicated P. Falciparum infection.BMC immunology · 2024Article
- Immunophenotyping of blood mononuclear cells fromJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2017Article
- CD4+ T cells apoptosis in Plasmodium vivax infection is mediated by activation of both intrinsic and extrinsic pathways.Malaria journal · 2015Article
- Analysis of lymphocytes in patients with Plasmodium vivax malaria and its relation to the annexin-A1 and IL-10.Malaria journal · 2013Article
- Predictive value of lymphocytopenia and the neutrophil-lymphocyte count ratio for severe imported malaria.Malaria journal · 2013Article
- Characterization of peripheral blood T lymphocyte subsets in Chinese rhesus macaques with repeated or long-term infection with Plasmodium cynomolgi.Parasitology research · 2012Article
- A -436C>A polymorphism in the human FAS gene promoter associated with severe childhood malaria.PLoS genetics · 2011Article
- Filarial infection suppresses malaria-specific multifunctional Th1 and Th17 responses in malaria and filarial coinfections.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Article
- Reduced CD3/TCR complex expression leads to immunosuppression during Plasmodium falciparum malaria.Parasitology research · 2009Article
- Apoptosis and the balance of homeostatic and pathologic responses to protozoan infection.Infection and immunity · 2003Review
- Malaria associated apoptosis is not significantly correlated with either parasitemia or the number of previous malaria attacks.Parasitology research · 2003Article
- Pneumococcal infections in humans are associated with increased apoptosis and trafficking of type 1 cytokine-producing T cells.Infection and immunity · 2002Article
- Increased levels of soluble CD30 in plasma of patients with Plasmodium falciparum malaria.Clinical and diagnostic laboratory immunology · 2002Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Available evidence suggests that Plasmodium falciparum malaria causes activation and reallocation of T cells, and that these in vivo primed cells re-emerge into the periphery following drug therapy. Here we have examined the cytokine production capacity and susceptibility to programmed cell death of peripheral T cells during and after the period of antimalarial treatment. A high proportion of peripheral CD3+ cells had an activated phenotype at and shortly after time of admission (day 0) and initiation of therapy. This activation peaked around day 2, and at this time-point peripheral T cells from the patients could be induced to produce cytokines at conditions of limited cytokine response in cells from healthy control donors. Activated CD8hi and TCR-gammadelta+ cells were the primary IFN-gamma producers, whereas CD4+ cells constituted an important source of TNF-alpha. The proportion of apoptotic T cells was elevated at admission and peaked 2 days later, while susceptibility to activation-induced cell death in vitro remained increased for at least 1 week after admission. Taken together, the data are consistent with the concept of malaria-induced reallocation of activated T cells to sites of inflammation, followed by their release back into the peripheral blood where they undergo apoptotic death to re-establish immunological homeostasis as inflammation subsides. However, the high proportion of pre-apoptotic cells from the time of admission suggests that apoptosis also contributes to the low frequency and number of T cells in the peripheral circulation during active disease.
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