The Journal of Experimental Medicine
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Published online 20 November 2000.
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© The Rockefeller University Press, 0022-1007/2000/11/1453/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 10, November 20, 2000 1453-1466

Original Article

Baff Mediates Survival of Peripheral Immature B Lymphocytes

Marcel Battena, Joanna Grooma, Teresa G. Cacherob, Fang Qianb, Pascal Schneiderc, Jurg Tschoppc, Jeffrey L. Browningb, and Fabienne Mackaya

a Department of Arthritis and Inflammation, The Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia
b Department of Immunology, Department of Inflammation, the Department of Cell Biology, and the Department of Protein Engineering, Biogen Incorporated, Cambridge, Massachusetts 02142
c Institute of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland
The Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, New South Wales 2010, Australia.61-2-9295-840461-2-9295-8414

B cell maturation is a very selective process that requires finely tuned differentiation and survival signals. B cell activation factor from the TNF family (BAFF) is a TNF family member that binds to B cells and potentiates B cell receptor (BCR)-mediated proliferation. A role for BAFF in B cell survival was suggested by the observation of reduced peripheral B cell numbers in mice treated with reagents blocking BAFF, and high Bcl-2 levels detected in B cells from BAFF transgenic (Tg) mice. We tested in vitro the survival effect of BAFF on lymphocytes derived from primary and secondary lymphoid organs. BAFF induced survival of a subset of splenic immature B cells, referred to as transitional type 2 (T2) B cells. BAFF treatment allowed T2 B cells to survive and differentiate into mature B cells in response to signals through the BCR. The T2 and the marginal zone (MZ) B cell compartments were particularly enlarged in BAFF Tg mice. Immature transitional B cells are targets for negative selection, a feature thought to promote self-tolerance. These findings support a model in which excessive BAFF-mediated survival of peripheral immature B cells contributes to the emergence and maturation of autoreactive B cells, skewed towards the MZ compartment. This work provides new clues on mechanisms regulating B cell maturation and tolerance.

Key Words: B cell maturation • autoimmunity • transitional B lymphocyte • spleen • antigen receptor

Abbreviations used in this paper: ANOVA, analysis of variance; BAFF, B cell activation factor from the TNF family; BCMA, B cell maturation antigen; BCR, B cell receptor; BM, bone marrow; FSC, forward light scatter; HSA, heat stable antigen; MLN, mesenteric LN; MZ, marginal zone; PI, propidium iodine; PLN, peripheral LN; SSC, side light scatter; T1, transitional immature B cell type 1; T2, transitional immature B cell type 2; TACI, transmembrane activator and calcium-modulating and cyclophilin ligand interactor; Tg, transgenic.

© 2000 The Rockefeller University Press


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