Conventional Light Chains Inhibit the Autonomous Signaling Capacity of the B Cell Receptor

Signals from the B cell antigen receptor (BCR), consisting of μ heavy chain (μHC) and conventional light chain (LC), and its precursor the pre-BCR, consisting of μHC and surrogate light chain (SLC), via the adaptor protein SLP-65 regulate the development and function of B cells. Here, we compare the effect of SLC and conventional LC expression on receptor-induced Ca2+ flux in B cells expressing an inducible form of SLP-65. We found that SLC expression strongly enhanced an autonomous ability of μHC to induce Ca2+ flux irrespective of additional receptor crosslinking. In contrast, LC expression reduced this autonomous μHC ability and resulted in antigen-dependent Ca2+ flux. These data indicate that autonomous ligand-independent signaling can be induced by receptor forms other than the pre-BCR. In addition, our data suggest that conventional LCs play an important role in the inhibition of autonomous receptor signaling, thereby allowing further B cell differentiation