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CUTTING EDGE |
5: A Paradigm Revisited1
Division of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger Center, University of Erlangen-Nürnberg, Erlangen, Germany
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-like transmembrane complex that is assembled from two µH chains (µHC) and two surrogate L chains consisting of the non-covalently associated polypeptides VpreB and
5. In
5-/- mice, pro-B cell maturation is impaired, but not completely blocked, implying that a µHC induces differentiation signals in the absence of
5. Using a mouse model, in which transgenic µHC expression can be controlled by tetracycline, we show that in the absence of
5, the transgenic µHC 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.
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