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通过红细胞介导微量注射来自T细胞因子刺激的B细胞的细胞质,在人B细胞系中诱导IgG

IgG induction in a human B cell line by red cell-mediated microinjection of the cytoplasm from T cell factor-stimulated B cells.

作者信息

Kishimoto T, Miki Y, Kishi H, Muraguchi A, Kishimoto S, Yamamura Y

出版信息

J Immunol. 1982 Oct;129(4):1367-71.

PMID:6980930
Abstract

Generation of a cytoplasmic factor(s) that induced IgG secretion in nonstimulated cells was demonstrated in TRF-stimulated cells by using red cell-mediated microinjection. Injection of the cytoplasm from a TRF-stimulated B lymphoblastoid cell line (CESS) into nonstimulated cells induced an increase of IgG-producing cells. Injection of TRF itself did not induce an increase of IgG-producing cells. Active substance(s) in the cytoplasm were generated at 2 hr after TRF stimulation, and IgG-producing cells reached their maximum level at 40 hr after injection of the factor(s). DFP, but not actinomycin D, inhibited the generation of the cytoplasmic factor(s). The activity of the cytoplasmic factor(s) was not destroyed by RNase and not absorbed with anti-IgG. These results suggested that binding of TRF with its acceptors induced the generation of the cytoplasmic factor(s) involved in the transmission of TRF-mediated signals from membrane to nuclei.

摘要

通过红细胞介导的显微注射,在经促甲状腺激素释放因子(TRF)刺激的细胞中证实了可诱导未受刺激细胞分泌IgG的细胞质因子的产生。将来自TRF刺激的B淋巴母细胞系(CESS)的细胞质注射到未受刺激的细胞中,可诱导产生IgG的细胞增加。注射TRF本身并不会诱导产生IgG的细胞增加。细胞质中的活性物质在TRF刺激后2小时产生,并且在注射该因子后40小时,产生IgG的细胞达到其最大水平。二异丙基氟磷酸(DFP)而非放线菌素D抑制了细胞质因子的产生。细胞质因子的活性不会被核糖核酸酶破坏,也不会被抗IgG吸附。这些结果表明,TRF与其受体的结合诱导了细胞质因子的产生,该因子参与了TRF介导的信号从膜到核的传递。

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