Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Uncertainty remains about the cellular origins of the earliest phase of the proinflammatory cytokine response to malaria. Here we show by fluorescence-activated cell sorter analysis that gammadelta T cells and CD14+ cells from nonimmune donors produce tumor necrosis factor and that gammadelta T cells also produce gamma interferon within 18 h of contact with mycoplasma-free Plasmodium falciparum-infected erythrocytes in vitro. This early cytokine response is more effectively induced by intact than by lysed parasitized erythrocytes. However, the IFN-gamma response to lysed parasites is considerably enhanced several days after peripheral blood mononuclear cells are primed with low numbers of intact parasitized erythrocytes, and in this case it derives from both alphabeta and gammadelta T cells. These data show that naïve gammadelta T cells can respond very rapidly to malaria infection but that malaria fever may involve a multistage process in which the priming of both gammadelta and alphabeta T-cell populations boosts the cytokine response to lysed parasite products released at schizont rupture.

Original publication

DOI

10.1128/IAI.69.4.2364-2371.2001

Type

Journal article

Journal

Infection and immunity

Publication Date

04/2001

Volume

69

Pages

2364 - 2371

Addresses

Department of Paediatrics, Oxford University, Oxford OX3 9DU, United Kingdom.

Keywords

Animals, Humans, Plasmodium falciparum, Tumor Necrosis Factor-alpha, Receptors, Antigen, T-Cell, alpha-beta, Interleukin-12, Cytokines, Adult, Interferon-gamma