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Blood, Vol. 94 No. 12 (December 15), 1999:
pp. 4210-4219
Interleukin-15 as an Activator of Natural Killer Cell-Mediated
Antiviral Response
Jean Gosselin,
Andru TomoÏu,
Robert C. Gallo, and
Louis Flamand
From the Laboratory of Viral Immunology, Laboratory of Virology,
Rheumatology and Immunology Research Center, Centre de Recherche du
CHUL and Anatomy and Physiology Department, Faculty of Medicine, Laval
University, Sainte-Foy, Quebec, Canada; and the Institute of Human
Virology, University of Maryland, Baltimore, MD.
Natural killer (NK) cells are large granular lymphocytes capable of
efficient killing of virus-infected and tumor cells in a major
histocompatibility complex-independent manner. The
cytotoxic killing potential of NK cells can be modulated by a variety
of factors, including cytokines such as interleukin-12 (IL-12), IL-15, and interferon (IFN). IL-15 also plays an important role in NK cell
development and survival. Killing of virally infected cells by NK cells
is likely to represent an important antiviral defense mechanism,
especially during the early phase of infection when antigen-specific
immunity has yet to be generated. In the present work, we studied the
potential of IL-15 to act as a modulator of NK cell-mediated antiviral
defense. Our results clearly indicate that IL-15 can curtail infections
by 3 human herpesviruses: Herpes simplex virus type 1, Epstein-Barr
virus, and human herpesvirus 6. The antiviral activity of IL-15 is
dose-, time-, and NK cell-dependent. IL-15-treated NK cells showed an
increased killing potential against a variety of cells, including
virus-infected target cells. Lastly, using highly purified cell
population, we report that IL-15 triggers the synthesis of IFN- from
both CD4+ and NK cells, which can act in both autocrine
and paracrine fashion to modulate NK cells cytotoxic potential. In
conclusion, IL-15 is a cytokine that can contribute to the
establishment of an antiviral state in 2 ways: first by increasing the
killing ability of NK cells and second by stimulating the synthesis and
secretion of IFN.
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