Kemp, K.Akanmori, B.D.Adabayeri, V.Goka, B.Q.Kurtzhals, J.A.L.Behr, C.Hviid, L.2019-02-282019-02-282002-01https://doi.org/10.1046/j.1365-2249.2002.01714.xVol. 127(1): pp 151-7http://ugspace.ug.edu.gh/handle/123456789/28449Available 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 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.enApoptosisCytokineCytometryFlowMalariaArticle