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ß Intermediate Cells Increase During Experimental Malaria Infection and Are Able to Exhibit Inhibitory Activity Against the Parasite Liver Stage In Vitro1
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Institut National de la Santé et de la Recherche Médicale U313, Immunobiologie Cellulaire et Moléculaire des Infections Parasitaires, CHU Pitié-Salpêtrière, Paris, France; and
Centre National de la Recherche Scientifique Unité de Recherche Associée 1961, Unité d’Immunochimie Analytique, Département d’Immunologie, Institut Pasteur, Paris, France
Experimental infection of C57BL/6 mice by Plasmodium
yoelii sporozoites induced an increase of
CD4-CD8- NK1.1+
TCR
ßint cells and a down-regulation of
CD4+ NK1.1+ TCRßint cells in
the liver during the acute phase of the infection. These cells showed
an activated CD69+, CD122+,
CD44high, and CD62Lhigh surface phenotype.
Analysis of the expressed TCRVß segment repertoire revealed that most
of the expanded CD4-CD8- (double-negative) T
cells presented a skewed TCRVß repertoire and preferentially used
Vß2 and Vß7 rather than Vß8. To get an insight into the function
of expanded NK1.1+ T cells, experiments were designed in
vitro to study their activity against P. yoelii liver
stage development. P. yoelii-primed CD3+
NK1.1+ intrahepatic lymphocytes inhibited parasite growth
within the hepatocyte. The antiplasmodial effector function of the
parasite-induced NK1.1+ liver T cells was almost totally
reversed with an anti-CD3 Ab. Moreover, IFN-
was in part
involved in this antiparasite activity. These results suggest that
up-regulation of CD4-CD8-
NK1.1+ ß T cells and down-regulation of
CD4+ NK1.1+ TCRßint cells may
contribute to the early immune response induced by the
Plasmodium during the prime
infection.
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