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Infection and Immunity, May 2001, p. 3190-3196, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3190-3196.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Perturbation and Proinflammatory Type Activation of Vdelta 1+ gamma delta T Cells in African Children with Plasmodium falciparum Malaria

Lars Hviid,1,* Jørgen A. L. Kurtzhals,1,2,3 Victoria Adabayeri,2 Severine Loizon,4 Kåre Kemp,1 Bamenla Q. Goka,2 Annick Lim,5 Odile Mercereau-Puijalon,4 Bartholomew D. Akanmori,3 and Charlotte Behr4

Centre for Medical Parasitology at Department of Infectious Diseases, Copenhagen University Hospital (Rigshospitalet) and Institute for Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark1; Department of Child Health, Korle-Bu Teaching Hospital, Accra,2 and Immunology Unit, Noguchi Memorial Institute for Medical Research, Legon,3 Ghana; and Unité d'Immunologie Moléculaires des Parasites, CNRS URA 1960,4 and Unité de Biologie Moleculaire du Gene,5 Institut Pastéur, Paris, France

Received 29 December 2000/Returned for modification 10 February 2001/Accepted 20 February 2001

gamma delta T cells have variously been implicated in the protection against, and the pathogenesis of, malaria, but few studies have examined the gamma delta T-cell response to malaria in African children, who suffer the large majority of malaria-associated morbidity and mortality. This is unfortunate, since available data suggest that simple extrapolation of conclusions drawn from studies of nonimmune adults ex vivo and in vitro is not always possible. Here we show that both the frequencies and the absolute numbers of gamma delta T cells are transiently increased following treatment of Plasmodium falciparum malaria in Ghanaian children and they can constitute 30 to 50% of all T cells shortly after initiation of antimalarial chemotherapy. The bulk of the gamma delta T cells involved in this perturbation expressed Vdelta 1 and had a highly activated phenotype. Analysis of the T-cell receptors (TCR) of the Vdelta 1+ cell population at the peak of their increase showed that all expressed Vgamma chains were used, and CDR3 length polymorphism indicated that the expanded Vdelta 1 population was highly polyclonal. A very high proportion of the Vdelta 1+ T cells produced gamma interferon, while fewer Vdelta 1+ cells than the average proportion of all CD3+ cells produced tumor necrosis factor alpha. No interleukin 10 production was detected among TCR-gamma delta + cells in general or Vdelta 1+ cells in particular. Taken together, our data point to an immunoregulatory role of the expanded Vdelta 1+ T-cell population in this group of semi-immune P. falciparum malaria patients.

* Corresponding author. Mailing address: Department of Infectious Diseases M7641, Rigshospitalet, Tagensvej 20, 2200 Copenhagen N, Denmark. Phone: (45) 35 45 79 57. Fax: (45) 35 45 76 44. E-mail: lhcmp{at}rh.dk.

Infection and Immunity, May 2001, p. 3190-3196, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3190-3196.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.