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水杨酸偶氮磺胺吡啶对接种到C3H小鼠盲肠腔内的抗原性肿瘤细胞免疫反应的影响。

The influence of salicyl-azo-sulfapyridine on the immune response to antigenic tumour cells inoculated into the coecal lumen of C3H mice.

作者信息

Laursen M L

出版信息

Scand J Gastroenterol. 1978;13(8):991-7. doi: 10.3109/00365527809181381.

Abstract

Pretreatment of C3H mice with salicyl-azo-sulfapyridine (SASP) was found to increase the susceptibility of the intestine to malignant ascites cells inoculated into the coecal lumen. The response to intestinal immunization was radically changed by prior treatment of mice with SASP. In non-treated animals protection against a subsequent graft followed the intracoecal inoculation of ascites tumour cells. By prior treatment of the mice with SASP the protective immune response was suppressed and some of the treated animals showed enhanced tumour growth of the challenging graft. The immunological enhancement induced in SASP-treated animals was transferable by spleen cells to untreated mice. In sera from SASP-treated and intestinally immunized animals were found factors which in a competitive manner interfered with the binding of antibodies to antigenic sites on the tumour cell membrane. It is proposed that treatment with SASP modifies the intestinal immunity by suppressing antibody production and increasing production of antigen-specific factors lacking some of the immunoglobulin determinants.

摘要

研究发现,用柳氮磺胺吡啶(SASP)预处理C3H小鼠会增加肠道对接种至盲肠腔的恶性腹水细胞的易感性。小鼠预先用SASP处理后,对肠道免疫的反应发生了根本性改变。在未处理的动物中,盲肠内接种腹水肿瘤细胞后可对随后的移植产生保护作用。预先用SASP处理小鼠会抑制保护性免疫反应,一些接受处理的动物显示出挑战性移植物的肿瘤生长增强。SASP处理的动物中诱导的免疫增强可通过脾细胞转移至未处理的小鼠。在SASP处理并经肠道免疫的动物血清中发现了一些因子,这些因子以竞争性方式干扰抗体与肿瘤细胞膜上抗原位点的结合。有人提出,SASP处理通过抑制抗体产生和增加缺乏某些免疫球蛋白决定簇的抗原特异性因子的产生来改变肠道免疫。

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