Hoffmann A, Kerr S, Jellusova J, Zhang J, Weisel F, Wellmann U, Winkler T, Kneitz B, Crocker PR, Nitschke L (2007)
Publication Status: Published
Publication Type: Journal article
Publication year: 2007
Publisher: NATURE PUBLISHING GROUP
Book Volume: 8
Pages Range: 694-704
Journal Issue: 7
DOI: 10.1038/ni1480
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.
APA:
Hoffmann, A., Kerr, S., Jellusova, J., Zhang, J., Weisel, F., Wellmann, U.,... Nitschke, L. (2007). Siglec-G is a B1 cell-inhibitory receptor that controls expansion and calcium signaling of the B1 cell population. Nature Immunology, 8(7), 694-704. https://dx.doi.org/10.1038/ni1480
MLA:
Hoffmann, Anja, et al. "Siglec-G is a B1 cell-inhibitory receptor that controls expansion and calcium signaling of the B1 cell population." Nature Immunology 8.7 (2007): 694-704.
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