Specificity of the generation and expression of enhanced anti-plasmacytoma immunity by spleen cells from melphalan-treated MOPC-315 tumor bearers.
Specificity of the generation and expression of enhanced anti-plasmacytoma immunity by spleen cells from melphalan-treated MOPC-315 tumor bearers.
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来自经美法仑治疗的 MOPC-315 肿瘤携带者的脾细胞产生和表达增强的抗浆细胞瘤免疫的特异性。
DOI：
10.1007/bf00205549
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Barker,E
中科院分区：
文献类型：
--
作者：
Mokyr,MB;Barker,E
We have shown previously that low-dose melphalan (L-PAM) therapy of mice bearing a large MOPC-315 plasmacytoma enables their hitherto immunosuppressed spleen cells to exert potent anti-MOPC-315 cytotoxicity following in vitro immunization with MOPC-315 tumor cells [3]. Here we show that, following in vitro immunization with MOPC-315 tumor cells, spleen cells from such L-PAM-treated MOPC-315 tumor bearers exhibited enhanced T-cell-mediated cytotoxicity not only against the MOPC-315 tumor, but also against another plasmacytoma (MOPC-104E) possessing surface immunoglobulin (SIg) of a different idiotype than the MOPC-315 cells, as well as against a variant of the MOPC-315 tumor which does not produce nor possess SIg (SIg−MOPC-315). The enhanced cytotoxicity was directed against target antigens which are not expressed on the surface of the syngeneic WEHI 22.1 thymoma or the natural killer-sensitive YAC-1 cells. Plasmacytoma shared antigens, other than immunoglobulins, were able to stimulate spleen cells from L-PAM-cured MOPC-315 tumor bearers to generate in vitro a secondary type anti-plasmacytoma cytotoxic response. L-PAM-cured MOPC-315 tumor bearers exhibited in vivo immunity against SIg−MOPC-315 tumor cells, which was sufficiently triggered by the SIg−cells to bring about the rejection of a challenge of at least 100-fold the minimal lethal tumor dose of the SIg−MOPC-315 cells. Thus, SIg−MOPC-315 tumor cells present among SIg+tumor cells in the parental MOPC-315 tumor inoculum [9, 26] can be eradicated in the L-PAM-treated MOPC-315 tumor bearers by the immune response to SIg+tumor cells as well as by the immune response to SIg−tumor cells themselves.
