Ray P K, Bandyopadhyay S K
Immunol Commun. 1983 Oct;12(5):453-64. doi: 10.3109/08820138309051962.
Intravenous inoculations of purified Protein A of Staphylococcus aureus Cowan I cause significant (p less than 0.01) regression of di-methyl-benz-anthracene (DMBA)-induced mammary adenocarcinomas in Sprague-Dawley rats. Direct tumor cell counts of treated tumors showed fewer (p less than 0.005) viable tumor cells than did tumors from untreated controls. Plasma immunoglobulin G concentration showed a significant (p less than 0.05) increase compared to that of controls. However, the concentration of immune complexes and percentages of T-rosettes did not change. Peripheral blood mononuclear cells (PBMNC) from treated animals showed increased cytotoxicity (p less than 0.005) compared to that of controls. Plasma of treated animals potentiated PBMNC cytotoxicity (p less than 0.05) and showed increased antibody and complement-mediated cytotoxicity (p less than 0.025). The exact mechanism of protein A-induced potentiation of anti-tumor immune reactivities leading to tumoricidal response is not known. However, our data are suggestive of the involvement of both cellular and humoral immunity of the host in the tumor regressive phenomenon.
静脉注射纯化的金黄色葡萄球菌考恩I型蛋白A可使斯普拉格-道利大鼠二甲基苯并蒽（DMBA）诱导的乳腺腺癌显著（p<0.01）消退。对治疗后的肿瘤进行直接肿瘤细胞计数显示，与未治疗对照组的肿瘤相比，存活肿瘤细胞更少（p<0.005）。血浆免疫球蛋白G浓度与对照组相比显著（p<0.05）升高。然而，免疫复合物的浓度和T花环百分比没有变化。与对照组相比，治疗动物的外周血单核细胞（PBMNC）显示细胞毒性增加（p<0.005）。治疗动物的血浆增强了PBMNC的细胞毒性（p<0.05），并显示抗体和补体介导的细胞毒性增加（p<0.025）。蛋白A诱导的抗肿瘤免疫反应增强导致杀肿瘤反应的确切机制尚不清楚。然而，我们的数据表明宿主的细胞免疫和体液免疫都参与了肿瘤消退现象。
