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克隆巨噬细胞杂交瘤的功能分析。VII. 抑制性T细胞诱导活性的调节。

Functional analysis of cloned macrophage hybridomas. VII. Modulation of suppressor T cell-inducing activity.

作者信息

Ishikura H, Jayaraman S, Kuchroo V, Diamond B, Saito S, Dorf M E

机构信息

Department of Pathology, Harvard Medical School, Boston, MA 02115.

出版信息

J Immunol. 1989 Jul 15;143(2):414-9.

PMID:2525585
Abstract

We have previously characterized a macrophage hybridoma clone, termed clone 59, which induced immunity but consistently failed to induce Ts responses. Macrophage 59 cells were cultured with supernatants from several activated T cell clones to determine if lymphokines could modulate the activity of this macrophage hybridoma to generate effector Ts. Culture supernatants from Th1 clones and from one atypical IL-4 and IFN-gamma-producing T cell clone successfully modulated clone 59 cells to induce effector Ts cells. In contrast, supernatants from activated Th2 cells failed to generate Ts-inducing activity in macrophage 59 cells. Culture with recombinant derived IFN-gamma was sufficient to cause modulation of Ts-inducing activity in macrophage 59 cells. The data imply that the differential functional activities ascribed to various macrophage hybridoma clones reflect macrophage heterogeneity instead of independent macrophage lineages. The suppression induced by clone 59 macrophages was genetically restricted to the putative I-J region. The ability of IFN-gamma containing supernatants to endow macrophage 59 with the capacity to induce effector suppressor cells was specifically abrogated by addition of an anti-IJk-idiotype antibody, which also reacts with IJ-interaction molecules, indicating that the mechanism of modulation most likely involves expression of IJ-interaction molecule determinants on antigen presenting cells.

摘要

我们之前鉴定了一个巨噬细胞杂交瘤克隆,称为59克隆,它能诱导免疫,但始终无法诱导Ts反应。用几种活化T细胞克隆的上清液培养巨噬细胞59,以确定淋巴细胞因子是否能调节该巨噬细胞杂交瘤的活性,从而产生效应性Ts细胞。来自Th1克隆以及一个产生非典型IL-4和IFN-γ的T细胞克隆的培养上清液成功地调节了59克隆细胞,使其诱导效应性Ts细胞。相反,活化Th2细胞的上清液未能在巨噬细胞59中产生诱导Ts的活性。用重组衍生的IFN-γ培养足以导致巨噬细胞59中诱导Ts活性的调节。数据表明,归因于各种巨噬细胞杂交瘤克隆的不同功能活性反映了巨噬细胞的异质性,而非独立的巨噬细胞谱系。59克隆巨噬细胞诱导的抑制在遗传上局限于假定的I-J区域。加入一种抗IJk-独特型抗体可特异性消除含IFN-γ的上清液赋予巨噬细胞59诱导效应性抑制细胞的能力,该抗体也与IJ相互作用分子反应,这表明调节机制很可能涉及抗原呈递细胞上IJ相互作用分子决定簇的表达。

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