Briskin M, Kuwabara M D, Sigman D S, Wall R
Molecular Biology Institute, UCLA School of Medicine, University of California 90024.
Science. 1988 Nov 18;242(4881):1036-7. doi: 10.1126/science.3143155.
The induction of immunoglobulin kappa light chain expression in 70Z/3 pre-B cells treated with bacterial lipopolysaccharide (LPS) requires the activation of the B cell-specific factor NF-kappa B, which binds to the kappa enhancer motif, GGGACTTTCC. This sequence alone can function as a tissue-specific enhancer for LPS-induced gene expression. A potent inhibitor of B lymphopoiesis [transforming growth factor-beta (TGF-beta)] was used to explore the mechanisms in the activation of kappa transcription by LPS and by interferon-gamma (IFN-gamma). TGF-beta inhibited LPS-induced kappa transcription but not the activation and in vitro binding of NF-kappa B. This indicates that NF-kappa B activation, while necessary, is not sufficient for LPS-induced kappa transcription. TGF-beta had no effect on IFN-gamma-induced kappa transcription, and NF-kappa B was not activated by IFN-gamma. These results reveal that LPS and IFN-gamma activate transcription through different mechanisms.
在用细菌脂多糖(LPS)处理的70Z/3前B细胞中,免疫球蛋白κ轻链表达的诱导需要激活B细胞特异性因子NF-κB,该因子与κ增强子基序GGGACTTTCC结合。仅该序列就可作为LPS诱导基因表达的组织特异性增强子。一种有效的B淋巴细胞生成抑制剂[转化生长因子-β(TGF-β)]被用于探究LPS和干扰素-γ(IFN-γ)激活κ转录的机制。TGF-β抑制LPS诱导的κ转录,但不抑制NF-κB的激活及体外结合。这表明NF-κB激活虽然是必需的,但不足以促进LPS诱导的κ转录。TGF-β对IFN-γ诱导的κ转录没有影响,且NF-κB不会被IFN-γ激活。这些结果揭示LPS和IFN-γ通过不同机制激活转录。