Goldrosen M H, Russo A J, Howell J H, Leveson S H, Holyoke E D
Cancer Res. 1979 Feb;39(2 Pt 2):587-92.
To study the cellular basis for specific antigen-induced leukocyte adherence inhibition, enriched populations of B-cells, T-cells, and monocytes were prepared by a two-stage adherence separation procedure from spleen cells of normal C57BL/6J mice and mice bearing progressively growing MCA-38 tumors. The reactor cell undergoing specific antigen-induced adherence inhibition was identified as a monocyte (esterase positive, did not respond to mitogens, and did not bear Thy 1.2 antigen or surface immunoglobulin). Furthermore, an enriched population of MCA-38-sensitized B-cells could program normal monocytes to undergo specific antigen-induced adherence inhibition. In contrast, enriched populations of MCA-38-sensitized T-cells could not program normal nylon wool-adherent cells to undergo antigen-specific adherence inhibition. Programming of normal monocytes by MCA-38-sensitized B-cells occurs through a soluble mediator and not by direct cell contact. The soluble mediator appears to be immunoglobulin in nature and induced both adherence inhibition and the inhibition of adherence. Thus, in this murine tumor model, leukocyte adherence inhibition appears to be due to programming of monocytes by a secretory product of specifically sensitized B-cells.
为研究特异性抗原诱导的白细胞黏附抑制的细胞基础,通过两阶段黏附分离程序,从正常C57BL/6J小鼠及携带进行性生长的MCA-38肿瘤的小鼠脾脏细胞中制备了富集的B细胞、T细胞和单核细胞群体。经历特异性抗原诱导黏附抑制的反应细胞被鉴定为单核细胞(酯酶阳性,对有丝分裂原无反应,不携带Thy 1.2抗原或表面免疫球蛋白)。此外,富集的MCA-38致敏B细胞群体可使正常单核细胞发生特异性抗原诱导的黏附抑制。相比之下,富集的MCA-38致敏T细胞群体不能使正常尼龙毛黏附细胞发生抗原特异性黏附抑制。MCA-38致敏B细胞对正常单核细胞的编程是通过可溶性介质而非直接细胞接触实现的。该可溶性介质在性质上似乎是免疫球蛋白,可诱导黏附抑制和对黏附的抑制。因此,在这个小鼠肿瘤模型中,白细胞黏附抑制似乎是由于特异性致敏B细胞的分泌产物对单核细胞进行编程所致。