Malaria-induced increase of splenic γδ T cells in humans, monkeys, and mice

Shusuke Nakazawa, Arthur E. Brown, Yoshimasa Maeno, C. Dahlem Smith, Masamichi Aikawa

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

The number and distribution of γδ T cells in spleens from patients who died of cerebral malaria and from rhesus monkeys severely infected with Plasmodium coatneyi were examined by immunocytochemistry. γδ T cells were significantly increased in these spleens. In a rodent malaria model using Plasmodium chabaudi adami, an avirulent strain of murine malaria parasites, the degree of parasitemia appears to be modulated by the number of γδ T cells in the spleen. As parasitemia increases, these T cells increase in number. At some critical point, γδ T cells in collaboration with macrophages and αβ T cells apparently start to clear parasitized erythrocytes from the blood, leading to an abatement of the parasitemia, which is followed by a reduction in the number of γδ T cells. This γδ T cell phenomenon may be responsible for the self-limiting infection in mice.

Original languageEnglish
Article number71101
Pages (from-to)391-398
Number of pages8
JournalExperimental Parasitology
Volume79
Issue number3
DOIs
Publication statusPublished - 01-01-1994

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Malaria
Haplorhini
T-Lymphocytes
Parasitemia
Spleen
Plasmodium chabaudi
Cerebral Malaria
Plasmodium
Macaca mulatta
Rodentia
Parasites
Erythrocytes
Immunohistochemistry
Macrophages
Infection

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Immunology
  • Infectious Diseases

Cite this

Nakazawa, Shusuke ; Brown, Arthur E. ; Maeno, Yoshimasa ; Smith, C. Dahlem ; Aikawa, Masamichi. / Malaria-induced increase of splenic γδ T cells in humans, monkeys, and mice. In: Experimental Parasitology. 1994 ; Vol. 79, No. 3. pp. 391-398.
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Malaria-induced increase of splenic γδ T cells in humans, monkeys, and mice. / Nakazawa, Shusuke; Brown, Arthur E.; Maeno, Yoshimasa; Smith, C. Dahlem; Aikawa, Masamichi.

In: Experimental Parasitology, Vol. 79, No. 3, 71101, 01.01.1994, p. 391-398.

Research output: Contribution to journalArticle

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