| First Author | Bossen C | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 3 | Pages | 787-97 |
| PubMed ID | 21287546 | Mgi Jnum | J:177020 |
| Mgi Id | MGI:5293305 | Doi | 10.1002/eji.201040591 |
| Citation | Bossen C, et al. (2011) Mutation of the BAFF furin cleavage site impairs B-cell homeostasis and antibody responses. Eur J Immunol 41(3):787-97 |
| abstractText | 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 ( approximately 5-fold) of fmBAFF alone generated intermediate levels of B cells without improving humoral responses to immunization. Processed BAFF was however important for B-cell homeostasis, as peripheral B-cell populations and antibody responses were readily restored by administration of soluble BAFF trimers in BAFF-deficient mice. However, the rescue of CD23 expression in B cells of BAFF-deficient mice required both soluble BAFF trimers and fmBAFF, or a polymeric form of soluble BAFF (BAFF 60-mer). These results point to a predominant role of processed BAFF for B-cell homeostasis and function, and indicate possible accessory roles for membrane-bound BAFF. |
