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 Blood, 1 May 2008, Vol. 111, No. 9, pp. 4627-4636.
Prepublished online as a Blood First Edition Paper on March 4, 2008; DOI 10.1182/blood-2007-12-128140.

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IMMUNOBIOLOGY

A critical role of Rap1b in B-cell trafficking and marginal zone B-cell development

Yuhong Chen1, Mei Yu1,2, Andrew Podd1,3, Renren Wen1, Magdalena Chrzanowska-Wodnicka1, Gilbert C. White1, and Demin Wang1,3

1 Blood Research Institute, BloodCenter of Wisconsin, Milwaukee; 2 State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, People's Republic of China; and 3 Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee

B-cell development is orchestrated by complex signaling networks. Rap1 is a member of the Ras superfamily of small GTP-binding proteins and has 2 isoforms, Rap1a and Rap1b. Although Rap1 has been suggested to have an important role in a variety of cellular processes, no direct evidence demonstrates a role for Rap1 in B-cell biology. In this study, we found that Rap1b was the dominant isoform of Rap1 in B cells. We discovered that Rap1b deficiency in mice barely affected early development of B cells but markedly reduced marginal zone (MZ) B cells in the spleen and mature B cells in peripheral and mucosal lymph nodes. Rap1b-deficient B cells displayed normal survival and proliferation in vivo and in vitro. However, Rap1b-deficient B cells had impaired adhesion and reduced chemotaxis in vitro, and lessened homing to lymph nodes in vivo. Furthermore, we found that Rap1b deficiency had no marked effect on LPS-, BCR-, or SDF-1–induced activation of mitogen-activated protein kinases and AKT but clearly impaired SDF-1–mediated activation of Pyk-2, a key regulator of SDF-1–mediated B-cell migration. Thus, we have discovered a critical and distinct role of Rap1b in mature B-cell trafficking and development of MZ B cells.


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