Production of BSF-1 during an in vivo, T-dependent immune response.
Production of BSF-1 during an in vivo, T-dependent immune response.
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在体内 T 依赖性免疫反应过程中产生 BSF-1。
DOI：
10.4049/jimmunol.137.9.2878
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发表时间：
1986
影响因子：
4.4
通讯作者：
W. Paul
中科院分区：
文献类型：
--
作者：
F. Finkelman;J. Ohara;D. K. Goroff;J. Smith;N. Villacreses;J. Mond;W. Paul
BSF-1是一些T淋巴细胞肿瘤产生的细胞因子，已被证明与抗Ig抗体一起刺激B淋巴细胞增殖，独立诱导静息的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IgG 1或IgE分泌细胞。为了确定BSF-1是否可能在生理免疫应答过程中由正常淋巴细胞分泌，给BALB/c小鼠注射亲和纯化的抗小鼠IgD的山羊抗体（GaM δ），其诱导产生大的多克隆T依赖性IgG 1应答;制备来自这些小鼠的脾细胞的4小时培养上清液，通过分析这些上清液体外诱导BALB/cnu/nu脾细胞增加其细胞表面Ia表达的能力，测定这些上清液的BSF-1活性。在注射GaM δ抗体后4至8天从小鼠中取出的未分级脾细胞的培养上清液诱导B淋巴细胞表面Ia表达的显著增加;这些增加被单克隆抗BSF-1抗体阻断。来自未处理的BALB/c小鼠或来自未处理的或GaM δ抗体处理的BALB/c nu/nu小鼠的脾细胞的培养上清液诱导B细胞表面Ia表达的小至中度增加，并且GaM δ抗体本身诱导B细胞表面Ia表达的大幅增加;然而，这些增加未被单克隆抗BSF-1抗体显著阻断。来自未处理小鼠的富含T细胞的脾细胞的培养上清液诱导B细胞表面Ia表达的小幅增加，其被抗BSF-1抗体抑制，正如来自GaM δ注射后3天处死的小鼠的富含T细胞的脾细胞的培养上清液诱导的B细胞Ia表达的较大增加一样。另一方面，在处死前7天注射GaM δ抗体的BALB/c小鼠的T细胞耗尽的脾细胞不能产生具有BSF-1活性的培养上清液。从取自未处理小鼠或在处死前1至3天用GaM δ抗体处理的小鼠的脾细胞制备的上清液不阻断纯化的BSF-1诱导B细胞表面Ia表达增加的能力，因此不含BSF-1活性的抑制剂。（400字处截断摘要）
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)