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在体内T细胞依赖性免疫反应过程中BSF-1的产生。

Production of BSF-1 during an in vivo, T-dependent immune response.

作者信息

Finkelman F D, Ohara J, Goroff D K, Smith J, Villacreses N, Mond J J, Paul W E

出版信息

J Immunol. 1986 Nov 1;137(9):2878-85.

PMID:3489779
Abstract

BSF-1, a cytokine produced by some T lymphocyte tumors, has been shown to act with anti-Ig antibodies to stimulate B lymphocyte proliferation, to independently induce resting B lymphocytes to increase their expression of surface Ia antigen, and to induce some activated B lymphocytes to differentiate into IgG1- or IgE-secreting cells. To determine whether BSF-1 might be secreted by normal lymphoid cells in the course of a physiologic immune response, BALB/c mice were injected with an affinity-purified goat antibody to mouse IgD (GaM delta), which induces the generation of a large, polyclonal T-dependent IgG1 response; 4-hr culture supernatants of spleen cells from these mice were prepared, and these supernatants were assayed for BSF-1 activity by analyzing their ability to induce BALB/c nu/nu spleen cells to increase their expression of cell surface Ia in vitro. Culture supernatants of unfractionated spleen cells removed from mice 4 to 8 days after GaM delta antibody injection induced substantial increases in B lymphocyte surface Ia expression; these increases were blocked by a monoclonal anti-BSF-1 antibody. Culture supernatants of spleen cells from untreated BALB/c mice or from untreated or GaM delta antibody-treated BALB/c nu/nu mice induced small to moderate increases in B cell surface Ia expression, and GaM delta antibody itself induced large increases in B cell surface Ia expression; however, these increases were not significantly blocked by a monoclonal anti-BSF-1 antibody. A culture supernatant of T cell-enriched spleen cells from untreated mice induced small increases in B cell surface Ia expression that were inhibited by anti-BSF-1 antibody, as was the larger increase in B cell Ia expression induced by a culture supernatant of T cell-enriched spleen cells from mice sacrificed 3 days after GaM delta injection. On the other hand, T cell-depleted spleen cells from BALB/c mice injected with GaM delta antibody 7 days before sacrifice failed to generate culture supernatants with BSF-1 activity. Supernatants prepared from spleen cells taken from untreated mice or mice treated with GaM delta antibody 1 to 3 days before sacrifice did not block the ability of purified BSF-1 to induce an increase in B cell surface Ia expression, and thus did not contain inhibitors of BSF-1 activity.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

BSF-1是一种由某些T淋巴细胞肿瘤产生的细胞因子,已显示它与抗Ig抗体共同作用,刺激B淋巴细胞增殖,独立诱导静止的B淋巴细胞增加其表面Ia抗原的表达,并诱导一些活化的B淋巴细胞分化为分泌IgG1或IgE的细胞。为了确定在生理性免疫反应过程中正常淋巴细胞是否可能分泌BSF-1,给BALB/c小鼠注射了一种亲和纯化的抗小鼠IgD山羊抗体(GaMδ),该抗体可诱导产生大量多克隆T细胞依赖性IgG1反应;制备了这些小鼠脾脏细胞的4小时培养上清液,并通过分析其在体外诱导BALB/c裸鼠脾脏细胞增加细胞表面Ia表达的能力来检测这些上清液中的BSF-1活性。在注射GaMδ抗体后4至8天从小鼠体内取出的未分级脾脏细胞的培养上清液可诱导B淋巴细胞表面Ia表达大幅增加;这些增加被一种抗BSF-1单克隆抗体所阻断。未处理的BALB/c小鼠或未处理或经GaMδ抗体处理的BALB/c裸鼠的脾脏细胞培养上清液可诱导B细胞表面Ia表达有小到中等程度的增加,而GaMδ抗体本身可诱导B细胞表面Ia表达大幅增加;然而,这些增加未被抗BSF-1单克隆抗体显著阻断。未处理小鼠的富含T细胞的脾脏细胞培养上清液可诱导B细胞表面Ia表达有小幅度增加,该增加被抗BSF-1抗体所抑制,注射GaMδ后3天处死的小鼠的富含T细胞的脾脏细胞培养上清液所诱导的B细胞Ia表达的较大增加也被抑制。另一方面,在处死前7天注射GaMδ抗体的BALB/c小鼠的T细胞耗竭的脾脏细胞未能产生具有BSF-1活性的培养上清液。在处死前1至3天从未处理小鼠或经GaMδ抗体处理的小鼠获取脾脏细胞制备的上清液不能阻断纯化的BSF-1诱导B细胞表面Ia表达增加的能力,因此不含有BSF-1活性的抑制剂。(摘要截短为400字)

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