Eccles S A, Alexander P
Br J Cancer. 1974 Jul;30(1):42-9. doi: 10.1038/bjc.1974.111.
The effects of rat tumours of various macrophage contents on the syngeneic host's ability to produce either: (1) an inflammatory exudate in response to intraperitoneal oyster glycogen or (2) a cutaneous delayed hypersensitivity (DHS) response to PPD or SRBC after appropriate sensitization, were studied as a function of tumour growth.Both these reactions were found to be markedly decreased as the tumours grew. The suppression was greatest in animals bearing tumours of high macrophage content. The suppression of the DHS response could be reversed by a local injection of normal peritoneal macrophages with the eliciting antigen, and lymphocytes from tumour bearing animals exhibiting poor DHS responses were able to adoptively transfer DHS reactivity to normal unsensitized recipients. The monocyte infiltration in response to oyster glycogen was also decreased, and these data indicate a monocyte, rather than a lymphocyte defect in the tumour induced "anergy" in this system.
(1)对腹腔注射牡蛎糖原产生炎性渗出物的能力,或(2)在适当致敏后对结核菌素纯蛋白衍生物(PPD)或绵羊红细胞(SRBC)产生皮肤迟发型超敏反应(DHS)的能力,并将其作为肿瘤生长的函数进行研究。随着肿瘤生长,发现这两种反应均显著降低。在携带高巨噬细胞含量肿瘤的动物中,抑制作用最大。通过局部注射正常腹腔巨噬细胞和引发抗原,可以逆转DHS反应的抑制,并且来自表现出不良DHS反应的荷瘤动物的淋巴细胞能够将DHS反应性过继转移给正常未致敏的受体。对牡蛎糖原的单核细胞浸润也减少,这些数据表明在该系统中肿瘤诱导的“无反应性”中存在单核细胞缺陷,而非淋巴细胞缺陷。