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. 1997 Oct;65(10):4090–4093. doi: 10.1128/iai.65.10.4090-4093.1997

Rapid reemergence of T cells into peripheral circulation following treatment of severe and uncomplicated Plasmodium falciparum malaria.

L Hviid 1, J A Kurtzhals 1, B Q Goka 1, J O Oliver-Commey 1, F K Nkrumah 1, T G Theander 1
PMCID: PMC175588  PMID: 9317012

Abstract

Frequencies and absolute numbers of peripheral T-cell subsets were monitored closely following acute Plasmodium falciparum malaria in 22 Ghanaian children from an area of hyperendemicity for seasonal malaria transmission. The children presented with cerebral or uncomplicated malaria (CM or UM, respectively) or with severe malarial anemia. For all patients the frequencies and absolute numbers of peripheral T cells were lower than normal during the acute stage of disease. This lowering was most pronounced in the CM group and least pronounced in the UM group. Of particular interest, the CM patients showed markedly reduced frequencies of CD4+ cells, the number of which also normalized slower than in the other clinical groups. In all patients, the T-cell frequencies gradually approached normal values after the initiation of therapy, whereas the absolute numbers rapidly reverted from lower than normal to higher than normal before returning to steady-state levels. Furthermore, the initially reduced T-cell surface density of the T-cell receptor/CD3 complex, which rapidly normalized, was a general finding for all three clinical groups, suggesting a state of peripheral T-cell hyporesponsiveness during acute malaria. The data presented suggest a rapid therapy-induced reemergence of T cells that had been temporarily removed from the peripheral circulation as a consequence of the malaria attack and that the degree of the disease-induced T-cell reallocation correlates with disease severity.

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Selected References

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  1. Chougnet C., Tallet S., Ringwald P., Deloron P. Kinetics of lymphocyte subsets from peripheral blood during a Plasmodium falciparum malaria attack. Clin Exp Immunol. 1992 Dec;90(3):405–408. doi: 10.1111/j.1365-2249.1992.tb05859.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Elhassan I. M., Hviid L., Satti G., Akerstrom B., Jakobsen P. H., Jensen J. B., Theander T. G. Evidence of endothelial inflammation, T cell activation, and T cell reallocation in uncomplicated Plasmodium falciparum malaria. Am J Trop Med Hyg. 1994 Sep;51(3):372–379. doi: 10.4269/ajtmh.1994.51.372. [DOI] [PubMed] [Google Scholar]
  3. Gilbreath M. J., MacDermott R. P., Pavanand K., Phisphumvithi P., Kongchareon S., Wimonwattrawatee T. Deficiency of Con A-induced suppressor cell activity in peripheral blood mononuclear cells from Thai adults naturally infected with Plasmodium falciparum and Plasmodium vivax. Parasite Immunol. 1983 Sep;5(5):431–440. doi: 10.1111/j.1365-3024.1983.tb00758.x. [DOI] [PubMed] [Google Scholar]
  4. Grau G. E., Piguet P. F., Engers H. D., Louis J. A., Vassalli P., Lambert P. H. L3T4+ T lymphocytes play a major role in the pathogenesis of murine cerebral malaria. J Immunol. 1986 Oct 1;137(7):2348–2354. [PubMed] [Google Scholar]
  5. Greenwood B. M., Oduloju A. J., Stratton D. Lymphocyte changes in acute malaria. Trans R Soc Trop Med Hyg. 1977;71(5):408–410. doi: 10.1016/0035-9203(77)90039-6. [DOI] [PubMed] [Google Scholar]
  6. Ho M., Webster H. K., Green B., Looareesuwan S., Kongchareon S., White N. J. Defective production of and response to IL-2 in acute human falciparum malaria. J Immunol. 1988 Oct 15;141(8):2755–2759. [PubMed] [Google Scholar]
  7. Ho M., Webster H. K., Looareesuwan S., Supanaranond W., Phillips R. E., Chanthavanich P., Warrell D. A. Antigen-specific immunosuppression in human malaria due to Plasmodium falciparum. J Infect Dis. 1986 Apr;153(4):763–771. doi: 10.1093/infdis/153.4.763. [DOI] [PubMed] [Google Scholar]
  8. Hviid L., Theander T. G., Abdulhadi N. H., Abu-Zeid Y. A., Bayoumi R. A., Jensen J. B. Transient depletion of T cells with high LFA-1 expression from peripheral circulation during acute Plasmodium falciparum malaria. Eur J Immunol. 1991 May;21(5):1249–1253. doi: 10.1002/eji.1830210523. [DOI] [PubMed] [Google Scholar]
  9. Jakobsen P. H., Morris-Jones S., Theander T. G., Hviid L., Hansen M. B., Bendtzen K., Ridley R. G., Greenwood B. M. Increased plasma levels of soluble IL-2R are associated with severe Plasmodium falciparum malaria. Clin Exp Immunol. 1994 Apr;96(1):98–103. doi: 10.1111/j.1365-2249.1994.tb06237.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Josimovic-Alasevic O., Feldmeier H., Zwingenberger K., Harms G., Hahn H., Shrisuphanunt M., Diamantstein T. Interleukin 2 receptor in patients with localized and systemic parasitic diseases. Clin Exp Immunol. 1988 May;72(2):249–254. [PMC free article] [PubMed] [Google Scholar]
  11. Kremsner P. G., Bienzle U. Soluble CD8 antigen in Plasmodium falciparum malaria. J Infect Dis. 1989 Aug;160(2):357–358. doi: 10.1093/infdis/160.2.357. [DOI] [PubMed] [Google Scholar]
  12. Kurtzhals J. A., Rodrigues O., Addae M., Commey J. O., Nkrumah F. K., Hviid L. Reversible suppression of bone marrow response to erythropoietin in Plasmodium falciparum malaria. Br J Haematol. 1997 Apr;97(1):169–174. doi: 10.1046/j.1365-2141.1997.82654.x. [DOI] [PubMed] [Google Scholar]
  13. Langhorne J., Simon-Haarhaus B. Differential T cell responses to Plasmodium chabaudi chabaudi in peripheral blood and spleens of C57BL/6 mice during infection. J Immunol. 1991 Apr 15;146(8):2771–2775. [PubMed] [Google Scholar]
  14. Molyneux M. E., Taylor T. E., Wirima J. J., Borgstein A. Clinical features and prognostic indicators in paediatric cerebral malaria: a study of 131 comatose Malawian children. Q J Med. 1989 May;71(265):441–459. [PubMed] [Google Scholar]
  15. Neequaye J., Ofori-Adjei E., Ofori-Adjei D., Renner L. Comparative trial of oral versus intramuscular chloroquine in children with cerebral malaria. Trans R Soc Trop Med Hyg. 1991 Nov-Dec;85(6):718–722. doi: 10.1016/0035-9203(91)90425-x. [DOI] [PubMed] [Google Scholar]
  16. Nguyen-Dinh P., Greenberg A. E. Increased levels of released interleukin-2 receptors in Plasmodium falciparum malaria. J Infect Dis. 1988 Dec;158(6):1403–1404. doi: 10.1093/infdis/158.6.1403. [DOI] [PubMed] [Google Scholar]
  17. Rzepczyk C. M., Stamatiou S., Anderson K., Stowers A., Cheng Q., Saul A., Allworth A., McCormack J., Whitby M., Olive C. Experimental human Plasmodium falciparum infections: longitudinal analysis of lymphocyte responses with particular reference to gamma delta T cells. Scand J Immunol. 1996 Feb;43(2):219–227. doi: 10.1046/j.1365-3083.1996.d01-24.x. [DOI] [PubMed] [Google Scholar]
  18. Viola A., Lanzavecchia A. T cell activation determined by T cell receptor number and tunable thresholds. Science. 1996 Jul 5;273(5271):104–106. doi: 10.1126/science.273.5271.104. [DOI] [PubMed] [Google Scholar]
  19. Wells R. A., Pavanand K., Zolyomi S., Permpanich B., MacDermott R. P. Loss of circulating T lymphocytes with normal levels of B and 'null' lymphocytes in Thai adults with malaria. Clin Exp Immunol. 1979 Feb;35(2):202–209. [PMC free article] [PubMed] [Google Scholar]
  20. Wyler D. J. Peripheral lymphocyte subpopulations in human falciparum malaria. Clin Exp Immunol. 1976 Mar;23(3):471–476. [PMC free article] [PubMed] [Google Scholar]

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