Cutting edge:: Signaling and cell surface expression of a μH chain in the absence of λ5:: A paradigm revisited
Cutting edge:: Signaling and cell surface expression of a μH chain in the absence of λ5:: A paradigm revisited
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DOI：
10.4049/jimmunol.171.7.3343
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发表时间：
2003-10-01
影响因子：
4.4
通讯作者：
Jäck, HM
中科院分区：
文献类型：
--
作者：
Schuh, W;Meister, S;Jäck, HM
前B细胞受体(Pre-BCR)信号是前B细胞高效成熟的关键。Pre-BCR是由两个MUH链和两个代理L链组装而成的类Ig跨膜复合体，由非共价结合多肽VpreB和lambda5组成。在lambda5(-/-)小鼠中，前B细胞成熟受到损害，但并未完全被阻断，这意味着MUHC在缺少lambda5的情况下诱导分化信号。在四环素可控制转基因MUHC表达的小鼠模型中，我们发现在没有lambda5的情况下，转基因MUHC促进了前B细胞的体内分化，诱导了IL-7依赖的细胞生长，并在前B细胞表面表达。我们的发现不仅表明不完整的Pre-BCR可以启动信号，而且还挑战了IgHC必须与IgLC或SLC相关联才能获得运输和信号能力的范式。
Pre-B cell receptor (pre-BCR) signals are essential for pro-B cells to mature efficiently into pre-B cells. The pre-BCR is an Ig-Iike transmembrane complex that is assembled from two muH chains (muHC) and two surrogate L chains consisting of the non-covalently associated polypeptides VpreB and lambda5. In lambda5(-/-) mice, pro-B cell maturation is impaired, but not completely blocked implying that a muHC induces differentiation signals in the absence of lambda5. Using a mouse model, in which transgenic muHC expression can be controlled by tetracycline, we show that in the absence of lambda5, the transgenic muHC promotes in vivo differentiation of pro-B cells, induces IL-7-dependent cell growth, and is expressed on the surface of pre-B cells. Our findings not only show that an incomplete pre-BCR can initiate signals, but also challenge the paradigm that an IgHC must associate with an IgLC or a SLC to gain transport and signaling competency.