TY - JOUR
T1 - The opposite effect of tumor-infiltrating natural killer cells on in vivo priming of tumor-specific CD8+ T cells and CD4+ T cells
AU - Terao, Hiroshi
AU - Harada, Mamoru
AU - Kurosawa, Shin
AU - Shinomiya, Yoshihiro
AU - Ito, Osamu
AU - Tamada, Koji
AU - Takenoyama, Mitsuhiro
AU - Nomoto, Kikuo
N1 - Funding Information:
This study was supported in part by a grant from the Ministry of Education, Science and Culture.
PY - 1996/7
Y1 - 1996/7
N2 - Natural killer (NK) cells, which infiltrated the tumor site, were examined for their effects on the in vivo priming of tumor-specific CD8+ and CD4+ T cells. CD8+ T cells mere responsible for the activity of B16 melanoma-specific cytotoxic T lymphocytes (CTL). The in vivo depletion of NK cells with anti-NR1.1 monoclonal antibody (mAb), prior to B16-immunization, significantly decreased the capacity of the spleen cells (SC) to generate B16-specific CTL after in vitro restimulation. However, the CD8+ T cells of the SC from NK cell-depleted and subsequently B16-immunized mice increased their potential to become B16-specific CTL compared with those from the Bib-immunized mice. The tumor-infiltrating NK cells showed a low but significant degree of CTL activity against B16. In addition, the disrupted B16 melanoma cells demonstrated less of an ability to in vivo prime the tumor-specific CD8+ T cells. These findings thus suggest the possibility that the quick disruption of tumor cells by tumor-infiltrating NK cells consequently interfered with the in vivo priming of the tumor-specific CD8+ T cells. On the other hand, the CD4+ T cells of the SC from NK cell-depleted and subsequently B16-immunized mice showed less of a capacity to induce the tumor-specific CTL compared with those from B16-immunized mice. In addition, the delayed-type hypersensitivity response against B16 was significantly diminished by the in vivo depletion of NK cells prior to B16-immunization. These findings thus suggest that NK cells have a promoting effect on the in vivo priming of CD4+ T cells. Overall, however, our findings indicate that early-appearing tumor-infiltrating NK cells have an opposite effect on the in vivo priming of CD8+ and CD4+ T cells.
AB - Natural killer (NK) cells, which infiltrated the tumor site, were examined for their effects on the in vivo priming of tumor-specific CD8+ and CD4+ T cells. CD8+ T cells mere responsible for the activity of B16 melanoma-specific cytotoxic T lymphocytes (CTL). The in vivo depletion of NK cells with anti-NR1.1 monoclonal antibody (mAb), prior to B16-immunization, significantly decreased the capacity of the spleen cells (SC) to generate B16-specific CTL after in vitro restimulation. However, the CD8+ T cells of the SC from NK cell-depleted and subsequently B16-immunized mice increased their potential to become B16-specific CTL compared with those from the Bib-immunized mice. The tumor-infiltrating NK cells showed a low but significant degree of CTL activity against B16. In addition, the disrupted B16 melanoma cells demonstrated less of an ability to in vivo prime the tumor-specific CD8+ T cells. These findings thus suggest the possibility that the quick disruption of tumor cells by tumor-infiltrating NK cells consequently interfered with the in vivo priming of the tumor-specific CD8+ T cells. On the other hand, the CD4+ T cells of the SC from NK cell-depleted and subsequently B16-immunized mice showed less of a capacity to induce the tumor-specific CTL compared with those from B16-immunized mice. In addition, the delayed-type hypersensitivity response against B16 was significantly diminished by the in vivo depletion of NK cells prior to B16-immunization. These findings thus suggest that NK cells have a promoting effect on the in vivo priming of CD4+ T cells. Overall, however, our findings indicate that early-appearing tumor-infiltrating NK cells have an opposite effect on the in vivo priming of CD8+ and CD4+ T cells.
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U2 - 10.1016/S0171-2985(96)80037-4
DO - 10.1016/S0171-2985(96)80037-4
M3 - Article
C2 - 8877394
AN - SCOPUS:0029813682
VL - 195
SP - 172
EP - 186
JO - Immunobiology
JF - Immunobiology
SN - 0171-2985
IS - 2
ER -