First Author | Hoffmann A | Year | 2007 |
Journal | Nat Immunol | Volume | 8 |
Issue | 7 | Pages | 695-704 |
PubMed ID | 17572677 | Mgi Jnum | J:123353 |
Mgi Id | MGI:3718146 | Doi | 10.1038/ni1480 |
Citation | Hoffmann A, et al. (2007) Siglec-G is a B1 cell-inhibitory receptor that controls expansion and calcium signaling of the B1 cell population. Nat Immunol 8(7):695-704 |
abstractText | B1 cells are an important cell population for the production of natural antibodies and for antibacterial immunoglobulin responses. Here we identified the mouse protein Siglec-G as a B1 cell inhibitory receptor. Siglec-G was expressed in a B cell-restricted way, with large amounts present in B1 cells. When overexpressed, Siglec-G inhibited B cell receptor-mediated calcium signaling. Siglec-G-deficient mice had massive expansion of the B1a cell population, which began early in development and was B cell intrinsic. Siglec-G-deficient mice had higher titers of natural IgM antibodies but not a higher penetrance of IgG autoantibodies. Siglec-G-deficient B1 cells showed a strongly enhanced calcium signaling. Our results demonstrate that Siglec-G-dependent negative regulation exists in B1 cells, which may explain the naturally muted signaling response of B1 cells. |