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,
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Center for Pulmonary and Infectious Disease Control, and Departments of
Microbiology and Immunology and
Medicine, University of Texas Health Center, Tyler, TX 75708;
Department of Internal Medicine, University of North Texas Health Sciences Center, Fort Worth, TX 76107;
¶ Lautenberg Center for General and Tumor Immunology, Hebrew University-Hadassah Medical School, Jerusalem, Israel; and
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Department of Microbiology and Immunology, Faculty of Health Sciences, and Cancer Research Center, Ben Gurion University of the Negev, Beer Sheva, Israel
We used human tuberculosis as a model to investigate the role of NK
cytotoxic mechanisms in the immune response to intracellular infection.
Freshly isolated NK cells and NK cell lines from healthy donors lysed
Mycobacterium tuberculosis-infected monocytes to a
greater extent than uninfected monocytes. Lysis of infected monocytes
was associated with increased expression of mRNA for the NKp46
receptor, but not the NKp44 receptor. Antisera to NKp46 markedly
inhibited lysis of infected monocytes. NK cell-mediated lysis was not
due to reduced expression of MHC class I molecules on the surface of
infected monocytes or to enhanced production of IL-18 or IFN-
. NK
cell lytic activity against M. tuberculosis-infected
monocytes and NKp46 mRNA expression were reduced in tuberculosis
patients with ineffective immunity to M. tuberculosis
compared with findings in healthy donors. These observations suggest
that 1) the NKp46 receptor participates in NK cell-mediated lysis of
cells infected with an intracellular pathogen, and 2) the reduced
functional capacity of NK cells is associated with severe
manifestations of infectious disease.
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