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脂多糖诱导的小鼠B细胞白血病(BCL1)分化:表面和分泌型IgM的变化

LPS-induced differentiation of a murine B cell leukemia (BCL1): changes in surface and secreted IgM.

作者信息

Lafrenz D, Koretz S, Stratte P T, Ward R B, Strober S

出版信息

J Immunol. 1982 Sep;129(3):1329-35.

PMID:6980922
Abstract

We examined the effect of LPS-induced differentiation on surface and secreted IgM in a cloned BCL1 in vitro cell line. Incubation of this cell line with LPS resulted in a decrease in the amount of membrane IgM, measured by both immunofluorescence and immunoprecipitation, and an increase in IgM secretion, measured by plaque-forming cells (PFC). Activation to high rate secretion was independent of cell cycle in synchronized cells and was independent of DNA synthesis because PFC formation was not inhibited by hydroxyurea. Almost all cells in the in vitro line were shown to contain large quantities of intracytoplasmic IgM before LPS activation. Thus, it would appear that the in vitro cell line represents a partially activated stage of differentiation compared to normal resting B cells or to the in vivo line of BCL1. Analysis of the two forms of mRNA coding for membrane and secreted IgM showed that, at least for cells at the level of differentiation examined here, the control of membrane IgM expression is post-transcriptional. The differentiation of resting B cells to the plasma cell level appears to consist of multiple stages of differentiation. The present data suggest that LPS provides at least two signals of activation. One induces the resting cell to synthesize cytoplasmic IgM, increase surface IgM, and to begin cell division. The second induces the secretion of intracytoplasmic IgM associated with a decrease in surface IgM.

摘要

我们检测了脂多糖(LPS)诱导分化对克隆的BCL1体外细胞系表面和分泌型IgM的影响。用LPS培养该细胞系,通过免疫荧光和免疫沉淀法检测发现膜IgM量减少,通过空斑形成细胞(PFC)检测发现IgM分泌增加。在同步化细胞中,向高速率分泌的激活与细胞周期无关,且与DNA合成无关,因为羟基脲不会抑制PFC形成。体外细胞系中几乎所有细胞在LPS激活前都含有大量胞质内IgM。因此,与正常静息B细胞或体内BCL1细胞系相比,体外细胞系似乎代表了分化的部分激活阶段。对编码膜IgM和分泌型IgM的两种mRNA形式的分析表明,至少对于此处检测的分化水平的细胞来说,膜IgM表达的调控是转录后调控。静息B细胞向浆细胞水平的分化似乎由多个分化阶段组成。目前的数据表明,LPS至少提供两种激活信号。一种信号诱导静息细胞合成胞质内IgM、增加表面IgM并开始细胞分裂。第二种信号诱导胞质内IgM分泌,同时表面IgM减少。

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