Liver CD4-CD8- NK1.1+ TCR alpha beta intermediate cells increase during experimental malaria infection and are able to exhibit inhibitory activity against the parasite liver stage in vitro

• Published in: The Journal of immunology (1950) Vol. 164; no. 3; pp. 1463 - 1469
• Main Authors: Pied, S, Roland, J, Louise, A, Voegtle, D, Soulard, V, Mazier, D, Cazenave, P A
• Format: Journal Article
• Language: English
• Published: United States 01-02-2000
• Subjects: Animals; Antigens - biosynthesis; Antigens, Ly; Antigens, Surface; CD4 Antigens - biosynthesis; CD8 Antigens - biosynthesis; Cells, Cultured; Down-Regulation - immunology; Gene Expression Regulation - immunology; Genes, T-Cell Receptor beta; Lectins, C-Type; Liver - immunology; Liver - parasitology; Liver - pathology; Liver Diseases, Parasitic - immunology; Liver Diseases, Parasitic - metabolism; Liver Diseases, Parasitic - parasitology; Lymphocyte Count; Malaria - immunology; Malaria - metabolism; Malaria - parasitology; Mice; Mice, Inbred C57BL; NK Cell Lectin-Like Receptor Subfamily B; Plasmodium yoelii - growth & development; Plasmodium yoelii - immunology; Protein Biosynthesis; Proteins; Receptors, Antigen, T-Cell, alpha-beta - biosynthesis; Receptors, Antigen, T-Cell, alpha-beta - genetics; T-Lymphocyte Subsets - immunology; T-Lymphocyte Subsets - metabolism; T-Lymphocyte Subsets - parasitology; T-Lymphocytes, Regulatory - immunology; T-Lymphocytes, Regulatory - metabolism; T-Lymphocytes, Regulatory - parasitology
• ISSN: 0022-1767
• DOI: 10.4049/jimmunol.164.3.1463

Experimental infection of C57BL/6 mice by Plasmodium yoelii sporozoites induced an increase of CD4-CD8- NK1.1+ TCR alpha beta int cells and a down-regulation of CD4+ NK1.1+ TCR alpha beta int 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 TCRV beta segment repertoire revealed that most of the expanded CD4-CD8- (double-negative) T cells presented a skewed TCRV beta repertoire and preferentially used V beta 2 and V beta 7 rather than V beta 8. 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-gamma was in part involved in this antiparasite activity. These results suggest that up-regulation of CD4-CD8- NK1.1+ alpha beta T cells and down-regulation of CD4+ NK1.1+ TCR alpha beta int cells may contribute to the early immune response induced by the Plasmodium during the prime infection.