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Cytokine production and apoptosis among T cells from patients under treatment for Plasmodium falciparum malaria by K. Kemp; B. D. Akanmori; V. Adabayeri; B. Q. Goka; J. A. L. Kurtzhals; C. Behr; L. Hviid is a Immunology and Microbiology article available to read on EtoBox.

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## Summary 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-γδ+ cells were the primary IFN-γ producers, whereas CD4+ cells constituted an important source of TNF-α. 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

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Author

K. Kemp; B. D. Akanmori; V. Adabayeri; B. Q. Goka; J. A. L. Kurtzhals; C. Behr; L. Hviid

Publisher

Oxford University Press (OUP)

Published

2002

Language

EN

Field

Immunology and Microbiology (Life Sciences)