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Mol. Cell. Biol. doi:10.1128/MCB.02273-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Phospholipase C2 contributes to light chain gene activation and receptor editing

Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, Wisconsin 53226, USA; Dali University, Dali, Yunnan 671000, P.R. China; School of Preclinical Medicine, Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China; State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210093, P. R. China; Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA

^* To whom correspondence should be addressed. Email: demin.wang{at}bcw.edu.

	Abstract

Phospholipase C2 (PLC2) is critical for pre-B cell receptor (pre-BCR) and BCR signaling. Current studies discovered that PLC2-deficient mice had reduced immunoglobulin (Ig) light chain usage throughout B cell maturation stages, including transitional type 1 (T1), transitional type 2 (T2), and mature follicular B cells. The reduction of Ig rearrangement by PLC2 deficiency was not due to specifically increased apoptosis or decreased proliferation of mutant Ig⁺ B cells, as lack of PLC2 inflicted a similar effect on apoptosis and proliferation of both Ig⁺ and Ig⁺ B cells. Moreover, PLC2-deficient Ig^HEL transgenic B cells exhibited an impairment of antigen-induced receptor editing among both the endogenous and loci in vitro and in vivo. Importantly, PLC2 deficiency impaired BCR-induced expression of IRF-4 and IRF-8, the two transcription factors critical for and light chain rearrangements. Taken together, these data demonstrate that PLC2 signaling pathway plays a role in activation of light chain loci and contributes to receptor editing.

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