Fc gamma RIIb controls bone marrow plasma cell persistence and apoptosis
- Author(s)
- Xiang, Z; Cutler, AJ; Brownlie, RJ; Fairfax, K; Lawlor, KE; Severinson, E; Walker, EU; Manz, RA; Tarlinton, DM; Smith, KGC;
- Details
- Publication Year 2007-04,Volume 8,Issue #4,Page 419-429
- Journal Title
- NATURE IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- The survival of long-lived plasma cells, which produce most serum immunoglobulin, is central to humoral immunity. We found here that the inhibitory Fc receptor Fc gamma RIIb was expressed on plasma cells and controlled their persistence in the bone marrow. Crosslinking Fc gamma RIIb induced apoptosis of plasma cells, which we propose contributes to the control of their homeostasis and suggests a method for therapeutic deletion. Plasma cells from mice prone to systemic lupus erythematosus did not express Fc gamma RIIb and were protected from apoptosis. Human plasmablasts expressed Fc gamma RIIb and were killed by crosslinking, as were Fc gamma RIIb-expressing myeloma cells. Our results suggest that Fc gamma RIIb controls bone marrow plasma cell persistence and that defects in it may contribute to autoantibody production.
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- SYSTEMIC-LUPUS-ERYTHEMATOSUS; MEMORY B-CELLS; ANTIBODY-FORMING-CELLS; GERMINAL CENTER; AUTOIMMUNE-DISEASE; IMMUNE-RESPONSE; RECEPTOR EXPRESSION; PROMOTER HAPLOTYPE; MULTIPLE-MYELOMA; HUMORAL IMMUNITY
- Publisher's Version
- https://doi.org/10.1038/ni1440
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2007-04-01 12:00:00