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Exhibit Enhanced Tumor Growth and Metastasis: Impaired NK Cell Development and Recruitment1
,§
*
Laboratory of Molecular Immunoregulation and
Laboratory of Experimental Immunology, Division of Basic Sciences, and
Intramural Research Support Program, Science Applications International Corp.-Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702, and
§
Laboratory of Molecular Immunology, Engelhardt Institute of Molecular Biology and Belozersky Institute of Physico-Chemical Biology, Moscow, Russia
Mice deficient in lymphotoxin (LT)-
lack peripheral lymph nodes
and Peyer’s patches and have profound defects in development of
follicular dendritic cell networks, germinal center formation, and T/B
cell segregation in the spleen. Although LT is known to be expressed
by NK cells as well as T and B lymphocytes, the requirement of LT
for NK cell functions is largely unknown. To address this issue, we
have assessed NK cell functions in LT-deficient mice by evaluating
tumor models with known requirements for NK cells to control their
growth and metastasis. Syngeneic B16F10 melanoma cells inoculated s.c.
grew more rapidly in LT-/- mice than in the wild-type
littermates, and the formation of experimental pulmonary metastases was
significantly enhanced in LT-/- mice. Although
LT-/- mice exhibited almost a normal total number of
NK cells in spleen, they showed an impaired recruitment of NK cells to
lung and liver. Additionally, lytic NK cells were not efficiently
produced from LT-/- bone marrow cells in vitro in the
presence of IL-2 and IL-15. These data suggest that LT signaling may
be involved in the maturation and recruitment of NK cells and may play
an important role in antitumor surveillance.
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