The Journal of Experimental Medicine
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Published 3 December 2001. doi:10.1084/jem.194.11.1649
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© Rockefeller University Press, 0022-1007/2001/12/1649/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 11, December 3, 2001 1649-1660

Original Article

 Splenic T Zone Development Is B Cell Dependent

Vu N. Ngo1, Richard J. Cornall2 and Jason G. Cyster1

1 Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California San Francisco, San Francisco, CA 94143
2 Nuffield Department of Medicine, Oxford University, John Radcliffe Hospital, Headington, Oxford OX3 9DU, United Kingdom

Address correspondence to Jason G. Cyster, Department of Microbiology and Immunology, University of California San Francisco, 513 Parnassus Ave., San Francisco, CA 94143-0414. Phone: 415-502-6427; Fax: 415-502-8424; E-mail: cyster{at}itsa.ucsf.edu

The factors regulating growth and patterning of the spleen are poorly defined. We demonstrate here that spleens from B cell–deficient mice have 10-fold reduced expression of the T zone chemokine, CCL21, a threefold reduction in T cell and dendritic cell (DC) numbers, and reduced expression of the T zone stromal marker, gp38. Using cell transfer and receptor blocking approaches, we provide evidence that B cells play a critical role in the early postnatal development of the splenic T zone. This process involves B cell expression of lymphotoxin (LT){alpha}1ß2, a cytokine that is required for expression of CCL21 and gp38. Introduction of a B cell specific LT{alpha} transgene on to the LT{alpha}-deficient background restored splenic CCL21 and gp38 expression, DC numbers, and T zone size. This work also demonstrates that the role of B cells in T zone development is distinct from the effect of B cells on splenic T cell numbers, which does not require LT{alpha}1ß2. Therefore, B cells influence spleen T zone development by providing: (a) signals that promote T cell accumulation, and: (b) signals, including LT{alpha}1ß2, that promote stromal cell development and DC accumulation. Defects in these parameters may contribute to the immune defects associated with B cell deficiency in mice and humans.

Key Words: lymphotoxin • SLC • BLC • stromal cell • dendritic cell


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