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Maintenance of Surrogate Light Chain Expression Induces Developmental Delay in Early B Cell Compartment¹

Denise A. Martin^*, Liwei Lu, Marilia Cascalho and Gillian E. Wu^2,*

^* Department of Kinesiology and Health Science, York University, Toronto, Ontario, Canada; Immunology Division, Department of Pathology, University of Hong Kong, Hong Kong; and Department of Surgery, Immunology, and Pediatrics, Mayo Clinic College of Medicine, Rochester, MN 55905

The production of a mature B cell requires passage through a number of developmental checkpoints. The pre-BCR plays a critical role in passage through the pro-B cell/pre-B cell checkpoint, and thus plays a central role in regulating the differentiation of a B cell. Due to the significance of this receptor, it is imperative that pre-BCR expression and function are precisely regulated. In this study, we have investigated a system in which the regulation of the pre-BCR is altered. We have found that continued expression of components of the pre-BCR (5) resulted in a delay in the kinetics of B cell maturation. Pro-B cells from normal mouse bone marrow retrovirally infected with 5 exhibited a delay in differentiation. As compared with wild-type cells at the same time point, there is a reduction in the presence of cell surface markers that indicate developmental progression, and there is a 6- to 16-fold decrease in the production of Ig-positive cells in B cell maturation assays. The capacity to alter B cell progression by modifying and extending pre-BCR expression argues that the receptor and its associated signals play a unique role in directing developmental outcomes.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the Canadian Institutes for Health Research, the Arthritis Society, and the Terry Fox Marathon of Hope (to G.E.W.). D.A.M. is a recipient of a Canadian Institutes for Health Research Doctoral Research Award. Support was provided to M.C. by National Institutes of Health Grant NIH RO1 AI48602.

² Address correspondence and reprint requests to Dr. Gillian E. Wu, Department of Kinesiology and Health Science, York University, Toronto, Canada. E-mail address: gillwu{at}yorku.ca

³ Abbreviations used in this paper: MB, monoclonal B; LAM5, 5; EMP, empty; EGFP, enhanced GFP; HPRT, hypoxanthine guanine phosphoribosyltransferase; MIEV, murine stem cell virus-based internal ribosome entry site-EGFP virus.