Hijioka Kuniaki, Matsuo Susumu, Eto-Kimura Akiko, Takeshige Koichiro, Muta Tatsushi
Department of Molecular and Cellular Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Biochem Biophys Res Commun. 2007 May 4;356(2):476-80. doi: 10.1016/j.bbrc.2007.03.002. Epub 2007 Mar 7.
The nuclear IkappaB protein IkappaB-zeta is barely detectable in resting cells and is induced in macrophages and fibroblasts following stimulation of innate immunity via Toll-like receptors. The induced IkappaB-zeta associates with nuclear factor (NF)-kappaB in the nucleus and plays crucial roles in its transcriptional regulation. Here, we examined the induction of IkappaB-zeta in B lymphocytes, one of the major players in adaptive immunity. Upon crosslinking of the surface immunoglobulin complex, IkappaB-zeta mRNA was robustly induced in murine B-lymphoma cell line A20 cells. While the crosslinking activated NF-kappaB and induced its target gene, IkappaB-alpha, co-crosslinking of Fcgamma receptor IIB to the surface immunoglobulin complex inhibited NF-kappaB activation and the induction of IkappaB-zeta and IkappaB-alpha, suggesting critical roles for NF-kappaB in the induction. These results indicate that IkappaB-zeta is also induced by stimulation of B cell antigen receptor, suggesting that IkappaB-zeta is involved in the regulation of adaptive immune responses.
核内的IκB蛋白IκB-ζ在静息细胞中几乎检测不到，在巨噬细胞和成纤维细胞中，通过Toll样受体刺激先天免疫后可被诱导产生。诱导产生的IκB-ζ在细胞核中与核因子（NF）-κB结合，并在其转录调控中发挥关键作用。在此，我们研究了IκB-ζ在B淋巴细胞中的诱导情况，B淋巴细胞是适应性免疫的主要参与者之一。在表面免疫球蛋白复合物交联后，IκB-ζ mRNA在小鼠B淋巴瘤细胞系A20细胞中被强烈诱导。虽然交联激活了NF-κB并诱导了其靶基因IκB-α，但Fcγ受体IIB与表面免疫球蛋白复合物的共交联抑制了NF-κB的激活以及IκB-ζ和IκB-α的诱导，这表明NF-κB在诱导过程中起关键作用。这些结果表明，IκB-ζ也可通过B细胞抗原受体的刺激而被诱导产生，提示IκB-ζ参与适应性免疫反应的调控。
