The Journal of Experimental Medicine
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Published online 13 October 2003 doi:10.1084/jem.20030495
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© Rockefeller University Press, 0022-1007/2003/10/1157 $5.00
The Journal of Experimental Medicine, Volume 198, Number 8, 1157-1169

Normal Induction but Attenuated Progression of Germinal Center Responses in BAFF and BAFF-R Signaling–Deficient Mice

Ziaur SM. Rahman1, Sambasiva P. Rao2, Susan L. Kalled2 and Tim Manser1

1 Department of Microbiology and Immunology, The Kimmel Cancer Center, Jefferson Medical College, Philadelphia, PA 19017
2 Department of Immunology and Inflammation, Biogen Inc., Cambridge, MA 02142

Address correspondence to Tim Manser, Dept. of Microbiology and Immunology, and The Kimmel Cancer Center, Jefferson Medical College, Bluemle Life Sciences Bldg., 708, 233 South 10th St., Philadelphia, PA 19017-5541. Phone: (215) 503-4543; Fax: (215) 923-4153; email: manser{at}mail.jci.tju.edu

The factors regulating germinal center (GC) B cell fate are poorly understood. Recent studies have defined a crucial role for the B cell–activating factor belonging to TNF family (BAFF; also called BLyS) in promoting primary B cell survival and development. A role for this cytokine in antigen-driven B cell responses has been suggested but current data in this regard are limited. A BAFF receptor expressed by B cells (BAFF-R/BR3) is defective in A/WySnJ mice which exhibit a phenotype similar to BAFF-deficient (BAFF-/-) animals. Here, we show that although GC responses can be efficiently induced in both A/WySnJ and BAFF-/- mice, these responses are not sustained. In BAFF-/- mice, this response is rapidly attenuated and accompanied by perturbed follicular dendritic cell development and immune complex trapping. In contrast, analysis of the A/WySnJ GC response revealed a B cell autonomous proliferative defect associated with reduced or undetectable Ki67 nuclear proliferation antigen expression by GC B cells at all stages of the response. These data demonstrate a multifaceted role for the BAFF pathway in regulating GC progression.

Key Words: B cell development • germinal center response • B cell memory • immunodeficiency • FDC reticulum


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