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微白细胞粘附抑制。I.反应机制的细胞基础。

Micro-leukocyte adherence inhibition. I. Cellular basis of the mechanism of reactivity.

作者信息

Russo A J, Howell J H, Leveson S H, Holyoke E D, Goldrosen M H

出版信息

J Immunol. 1978 Nov;121(5):1914-9.

PMID:81856
Abstract

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. This programming could be abolished by pretreatment of the MCA-38 sensitized B cells with anti-immunoglobulin and complement (indirect cytotoxicity method). In contrast, enriched populations of MCA-38 sensitized T cells could not program normal nylon wool adherent cells to undergo antigen-specific adherence inhibition; and anti-Thy 1.2 serum and complement had no effect on specific antigen-induced adherence inhibition. Thus, in this murine tumor model, leukocyte adherence inhibition appears to be due to the programming of monocytes by sensitized B cells.

摘要

为了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小鼠和携带逐渐生长的MCA-38肿瘤的小鼠的脾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的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细胞群体可以使正常单核细胞进行特异性抗原诱导的黏附抑制。这种编程可以通过用抗免疫球蛋白和补体预处理MCA-38致敏B细胞来消除(间接细胞毒性方法)。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进行抗原特异性黏附抑制;抗Thy 1.2血清和补体对特异性抗原诱导的黏附抑制没有影响。因此,在这个小鼠肿瘤模型中,白细胞黏附抑制似乎是由于致敏B细胞对单核细胞的编程所致。

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