Maturation of Marginal Zone and Follicular B Cells Requires B Cell Activating Factor of the Tumor Necrosis Factor Family and Is Independent of B Cell Maturation Antigen

Author:

Schneider Pascal1,Takatsuka Hisakazu1,Wilson Anne2,Mackay Fabienne3,Tardivel Aubry1,Lens Susanne1,Cachero Teresa G.4,Finke Daniela5,Beermann Friedrich5,Tschopp Jürg1

Affiliation:

1. Institute of Biochemistry, BIL Biomedical Research Center, University of Lausanne, the

2. Ludwig Institute for Cancer Research, Lausanne Branch, University of Lausanne, Boveresses 155, CH-1066 Epalinges, Switzerland

3. Garvan Institute of Medical Research, St. Vincent Hospital, Darlinghurst NSW 2010, Sydney, Australia

4. Biogen, Department of Protein Chemistry, Cambridge, MA 02142

5. Swiss Institute for Experimental Cancer Research, Lausanne Branch, University of Lausanne, Boveresses 155, CH-1066 Epalinges, Switzerland

Abstract

B cells undergo a complex series of maturation and selection steps in the bone marrow and spleen during differentiation into mature immune effector cells. The tumor necrosis factor (TNF) family member B cell activating factor of the TNF family (BAFF) (BLyS/TALL-1) plays an important role in B cell homeostasis. BAFF and its close homologue a proliferation-inducing ligand (APRIL) have both been shown to interact with at least two receptors, B cell maturation antigen (BCMA) and transmembrane activator and cyclophilin ligand interactor (TACI), however their relative contribution in transducing BAFF signals in vivo remains unclear. To functionally inactivate both BAFF and APRIL, mice transgenic for a soluble form of TACI were generated. They display a developmental block of B cell maturation in the periphery, leading to a severe depletion of marginal zone and follicular B2 B cells, but not of peritoneal B1 B cells. In contrast, mice transgenic for a soluble form of BCMA, which binds APRIL, have no detectable B cell phenotype. This demonstrates a crucial role for BAFF in B cell maturation and strongly suggests that it signals via a BCMA-independent pathway and in an APRIL-dispensable way.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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