Blanchard, D K;
Stewart, W E;
Klein, T W;
Friedman, H;
Djeu, J Y
Cytolytic activity of human peripheral blood leukocytes against Legionella pneumophila-infected monocytes: characterization of the effector cell and augmentation by interleukin 2
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Media type:
E-Article
Title:
Cytolytic activity of human peripheral blood leukocytes against Legionella pneumophila-infected monocytes: characterization of the effector cell and augmentation by interleukin 2
Contributor:
Blanchard, D K;
Stewart, W E;
Klein, T W;
Friedman, H;
Djeu, J Y
Published:
The American Association of Immunologists, 1987
Published in:
The Journal of Immunology, 139 (1987) 2, Seite 551-556
Language:
English
DOI:
10.4049/jimmunol.139.2.551
ISSN:
1550-6606;
0022-1767
Origination:
Footnote:
Description:
Abstract The present study was an in vitro attempt to define the effector mechanisms against the intracellular bacterium Legionella pneumophila. Monocytes from human peripheral blood leukocytes (PBL) were infected in vitro with L. pneumophila and cultured for 2 days to allow intracellular replication of the bacterium. Cells were then labeled with 51Cr and used as targets in a 4-h 51Cr-release assay. We report here that autologous nonadherent PBL effectively lysed infected monocytes, and this activity was enhanced when the effector cells were precultured with IL 2 for 2 days. The IL 2-activated killer cells were also cytolytic against uninfected cultured monocytes, but cytotoxicity was higher against Legionella-infected target cells in a dose-dependent manner. The effector cells were located in Percoll density fractions that were enriched for large granular lymphocytes. The phenotype of the effector cell activated by IL 2 was determined to be OKM1+, OKT11+, partially Leu-11+, and negative for Leu-M1, OKT4, OKT8, and Leu-7, indicating that it is neither a T cell nor a monocyte, and is possibly and NK subset that is Leu-11+ and Leu-7-. Cold target inhibition studies indicated that a similar recognition structure is shared by both infected and uninfected monocytes, but differs from that on K562 tumor target cells. Thus, in addition to tumor surveillance and controlling viral infections, killer cells can be activated to provide protection against intracellular bacterial infections.