摘要
应用ＭＡ７３－２３４乳腺癌津白Ⅱ号小鼠动物模型，探讨了随病程进展而不断增大的肿瘤负荷对Ｍφ抗瘤效应如Ｍφ分泌的ＩＬ－１活性水平、Ｍφ吞噬功能ＭＭＡＤＣＣ效应的动态影响。结果发现，Ｍφ分泌的ＩＬ－１活性水平在病程早期即明显下降，提示该功能更易受到肿瘤负荷的影响，从而可能会中枢性地抑制宿主免疫系统抗肿瘤效应的发挥，成为逃避宿主免疫工攻击的分子机制之一；而Ｍφ吞噬功能、ＭＭＡＤＣＣ效应在病程早期或中期当肿瘤负荷较小时有所加强，而晚期在肿瘤负荷较大时则减弱。
One of the focus of tumor immunology is to study the mechanism of carcinoma immune escape. So we used the TA 2 mouse model, which bearing MA 73-234 breast cancer, to study the change of macrophage (Mψ) antitumor activity include Mψ phgocytosis test、the activity of interleukin-1 (IT-1) which are secreted by Mψ and Mψ mediated ADCC (MMADCC) along in the course of disease development. The results were as follows:the activity of(IL-1)which are secreted by Mψ was evidently decreased in early course of disease, suggest this function was easy inhibited by tumor,then centric inhibited the antitumor activity of host immune system perhaps was one of the molecular mechanism for tumor to escape the immune actived; the Mψ phagacytosis was one of the molecular mechanism for tumor to escape the immune actived; the Mψ phagacytosis test、MMADCC were increased in early course of disease, but were decreased in latter course of desease.
