| First Author | Montaudouin C | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 1 | Pages | 106-14 |
| PubMed ID | 23209322 | Mgi Jnum | J:190824 |
| Mgi Id | MGI:5449766 | Doi | 10.4049/jimmunol.1200907 |
| Citation | Montaudouin C, et al. (2013) Quorum Sensing Contributes to Activated IgM-Secreting B Cell Homeostasis. J Immunol 190(1):106-14 |
| abstractText | Maintenance of plasma IgM levels is critical for immune system function and homeostasis in humans and mice. However, the mechanisms that control homeostasis of the activated IgM-secreting B cells are unknown. After adoptive transfer into immune-deficient hosts, B lymphocytes expand poorly, but fully reconstitute the pool of natural IgM-secreting cells and circulating IgM levels. By using sequential cell transfers and B cell populations from several mutant mice, we were able to identify novel mechanisms regulating the size of the IgM-secreting B cell pool. Contrary to previous mechanisms described regulating homeostasis, which involve competition for the same niche by cells having overlapping survival requirements, homeostasis of the innate IgM-secreting B cell pool is also achieved when B cell populations are able to monitor the number of activated B cells by detecting their secreted products. Notably, B cell populations are able to assess the density of activated B cells by sensing their secreted IgG. This process involves the FcgammaRIIB, a low-affinity IgG receptor that is expressed on B cells and acts as a negative regulator of B cell activation, and its intracellular effector the inositol phosphatase SHIP. As a result of the engagement of this inhibitory pathway, the number of activated IgM-secreting B cells is kept under control. We hypothesize that malfunction of this quorum-sensing mechanism may lead to uncontrolled B cell activation and autoimmunity. |
