Geisberger Roland, Königsberger Sebastian, Achatz Gernot
University of Salzburg, Department of Molecular Biology, Division Allergy and Immunology Hellbrunnertsrasse 34, A-5020 Salzburg, Austria.
Immunol Lett. 2006 Feb 15;102(2):169-76. doi: 10.1016/j.imlet.2005.09.001. Epub 2005 Sep 29.
Signalling through the B cell antigen receptor (BCR) is required for peripheral B lymphocyte maturation, maintenance, activation and silencing. In mature B cells, the antigen receptor normally consists of two isotypes: membrane IgM and IgD (mIgM, mIgD). Although the signals initiated from both isotypes differ in kinetics and intensity, in vivo, the BCR of either isotype seems to be able to compensate for the loss of the other, reflected by the mild phenotypes of mice deficient for mIgM or mIgD. Thus, it is still unclear why mature B cells need expression of mIgD in addition to mIgM. In the present paper, we used the B cell line Bcl1 and investigated the isotype-specific antigen internalization in dependence of co-stimulation of the reciprocal isotype and analysed whether the signal initiated from mIgM is modulated through signalling from mIgD and vice versa. We clearly showed that cross-linkage of mIgM decreases the rate of mIgD mediated antigen internalization and interpret this influence as a unilateral mIgM mediated control on signals initiated at mIgD.
通过B细胞抗原受体(BCR)发出信号对于外周B淋巴细胞的成熟、维持、激活和沉默是必需的。在成熟B细胞中,抗原受体通常由两种同种型组成:膜IgM和IgD(mIgM、mIgD)。尽管从这两种同种型引发的信号在动力学和强度上有所不同,但在体内,任何一种同种型的BCR似乎都能够补偿另一种的缺失,这在缺乏mIgM或mIgD的小鼠的轻微表型中得到了体现。因此,目前仍不清楚为什么成熟B细胞除了表达mIgM外还需要表达mIgD。在本文中,我们使用B细胞系Bcl1,研究了同种型特异性抗原内化对相互同种型共刺激的依赖性,并分析了从mIgM引发的信号是否通过mIgD的信号传导进行调节,反之亦然。我们清楚地表明,mIgM的交联降低了mIgD介导的抗原内化速率,并将这种影响解释为mIgM对mIgD引发的信号的单向控制。