Journal article

Mutation of the BAFF furin cleavage site impairs B-cell homeostasis and antibody responses

Claudia Bossen, Aubry Tardivel, Laure Willen, Carrie A Fletcher, Mai Perroud, Friedrich Beermann, Antonius G Rolink, Martin L Scott, Fabienne Mackay, Pascal Schneider



B-cell-activating factor of the TNF family (BAFF)/BLyS contributes to B-cell homeostasis and function in the periphery. BAFF is expressed as a membrane-bound protein or released by proteolytic cleavage, but the functional importance of this processing event is poorly understood. Mice expressing BAFF with a mutated furin consensus cleavage site, i.e. furin-mutant BAFF (fmBAFF), were not different from BAFF-deficient mice with regard to their B-cell populations and responses to immunization. It is however noteworthy that an alternative processing event releases some soluble BAFF in fmBAFF mice. Mild overexpression (∼ 5-fold) of fmBAFF alone generated intermediate levels of B cells without impr..

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University of Melbourne Researchers


Funding Acknowledgements

We thank Olivier Donze and Toufik Abbas-Terki (Adipogen, Epalinges, Switzerland) for performing endotoxin tests, Virginie Petrilli, Kate Schroder and Greta Guarda (University of Lausanne, Switzerland) for their help with in vitro differentiation of DCs and CD23 qPCR, Sabrina Guichard (EPFL, Lausanne) for oocyte microinjections and Damien Saulep (Monash University, Melbourne Australia) for expert technical help. F.M. is supported by the National Health and Medical Research Council of Australia. This work was supported by grants from the Swiss National Science Foundation (to P.S.).