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角叉菜胶、聚乙烯吡咯烷酮和荷瘤小鼠血清对小鼠切除或丝裂霉素C处理的肿瘤细胞诱导的免疫的影响。

Effects of carrageenan, PVP and tumour-bearer serum on immunity induced by excision or mitomycin C-treated tumour cells in mice.

作者信息

Kearney R, Wu R L, Orr F

出版信息

Br J Cancer. 1979 Jun;39(6):648-58. doi: 10.1038/bjc.1979.116.

Abstract

Carrageenan (Cg) was tested for its effects on the growth of, and immunity to, 2 methylcholanthrene-induced syngeneic murine fibrosarcomas (H1 and H2). The tumours were found not to share major tumour-specific transplantation antigens. H2 appeared more immunogenic than H1. In contrast to H1, immunity induced by H2 was not affected by Cg, nor was its growth in Cg-treated normal mice augmented.Postoperative i.p. injections of Cg abolished the weak anti-H1 immunity produced by H1 tumour excision. Furthermore, the subsequent growth of the H1 tumour challenge in the Cg-treated immune mice was significantly greater than the augmented growth in Cg-treated normal mice. The Prior administration of the macrophage-stabilizing agent polyvinylpyrrolidone (PVP) to immune mice significantly reduced the augmenting effect of Cg. The growth-promoting effect of Cg on a secondary H1 tumour challenge in mice immunized by tumour excision was abolished by 10(6) MCT-H1 cells injected s.c. before Cg. In contrast to the immunity induced by tumour excision, Cg did not abolish the immunity induced by the injection of MCT-H1 cells.Passive administration of H1 tumour-bearer serum (TBS) did not enhance the growth of H1 cells in normal mice, nor did TBS abrogate the specific cell-mediated immunity (CMI) induced in vivo by MCT-H1 cells. However, TBS administered to Cg-treated, MCT-H1-immune mice abolished tumour immunity.We propose that TBS does not inhibit CMI in vivo provided that macrophages remain functional, but may do so when macrophages are rendered defective by antimacrophage agents or by products of neoplastic cells. Increasing the levels of specific effector cells can over-ride the inhibiting effects of TBS, even when defective macrophages are present.

摘要

测试了角叉菜胶(Cg)对2-甲基胆蒽诱导的同基因小鼠纤维肉瘤(H1和H2)生长及免疫的影响。发现这些肿瘤不共享主要的肿瘤特异性移植抗原。H2似乎比H1更具免疫原性。与H1相反,H2诱导的免疫不受Cg影响,其在经Cg处理的正常小鼠中的生长也未增强。术后腹腔注射Cg消除了H1肿瘤切除产生的微弱抗H1免疫。此外,在经Cg处理的免疫小鼠中,随后对H1肿瘤攻击的生长明显大于经Cg处理的正常小鼠中增强的生长。预先给免疫小鼠施用巨噬细胞稳定剂聚乙烯吡咯烷酮(PVP)可显著降低Cg的增强作用。在注射Cg之前皮下注射10(6) MCT-H1细胞可消除Cg对经肿瘤切除免疫的小鼠中二次H1肿瘤攻击的生长促进作用。与肿瘤切除诱导的免疫相反,Cg并未消除注射MCT-H1细胞诱导的免疫。被动给予H1荷瘤血清(TBS)不会增强正常小鼠中H1细胞的生长,TBS也不会消除MCT-H1细胞在体内诱导的特异性细胞介导免疫(CMI)。然而,给予经Cg处理、MCT-H1免疫的小鼠TBS可消除肿瘤免疫。我们提出,只要巨噬细胞保持功能,TBS在体内不会抑制CMI,但当巨噬细胞因抗巨噬细胞剂或肿瘤细胞产物而功能缺陷时可能会抑制。增加特异性效应细胞的水平可以克服TBS的抑制作用,即使存在功能缺陷的巨噬细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7b0/2009980/f1fd7321459d/brjcancer00152-0043-a.jpg

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