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류현열,Andrew C. von Eschenbach 고신대학교(의대) 고신대학교 의과대학 학술지 1995 고신대학교 의과대학 학술지 Vol.10 No.2
-Abstract- Natural killer (NK) cells that had infilterated renal cell carcinoma (RCC) proliferated vigorously in culture which activated interleukin-2 (IL-2) and lysed autologous tumor cells. We studied the susceptibility of RCC cells to NK cell lysis and their ability to stimulate proliferation and function of NK cells. Cells from primary culture of RCC (p-RCC cells) were significantly more susceptible to lysis mediated by human NK 3.3 clones than were cells from primary culture of metastatic melanomas. RCC cells clones was also susceptible to lysis by NK 3.3 clones and IL-2 activated peripheral blood lymphocytes (PBLs). Incubation of NK 3.3 clones with p-RCC cells in the absence of IL-2 induced proliferation of NK 3.3 clones, whereas incubation with cells from primary culture of metastatic melanomas, K 562 cells tested did not. The p-RCC cells from earlier passages were more potent inducers of NK-cell proliferation than were those from older passages. Cell-free culture supernatants of p-RCC cells with or without NK 3.3 clones failed to induce NK-cell proliferation. Incubation of NK cells purified from PBLs with p-RCC cells induced higher proliferation of the NK cells only in the presence of IL-2, whereas incubation with cells from primary culture of metastatic melanomas did not. In summary, these results suggest that RCC cells are able to activate NK cells, potentially through cell-to-cell interaction.
류현열,Eschenbach, Andrew C. von 고신대학교 의학부 1995 高神大學校 醫學部 論文集 Vol.10 No.2
Natural killer (NK) cells that had infilterated renal cell carcinoma(RCC) proliferated vigorously in culture which activated interleukin-2(IL-2) and lysed autologous tumor cells. We studied the susceptibility of RCC cells to NK-cell lysis and their ability to stimulate proliferation and function of NK cells. Cells from primary culture of RCC(p-RCC cells) were significantly more susceptible to lysis mediated by human NK3.3 clones than were cells from primary culture of metastatic melanomas. RCC cells clones was also susceptible to lysis by NK3.3 clones and IL-2 activated peripheral blood lymphocytes(PBLs). Incubation of NK3.3 clones with p-RCC cells in the absence of IL-2 induced proliferation of NK3.3 clones, whereas incubation with cells from primary culture of metastatic melanomas, K562 cells tested did not. The p-RCC cells from earlier passages were more potent inducers of NK-cell proliferation than were those from older passages. Cell-free culture supernatants of p-RCC cells with or without NK3.3 clones failed to induce NK-cell proliferation. Incubation of NK cells purified from PBLs with p-RCC cells induced higher proliferation of the NK cells only in the presence of IL-2, whereas incubation with cells from primary culture of metastatic melanomas did not. In summary, these results suggest that RCC cells are able to activate NK cells, potentially through cell-to-cell interaction.