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Journal Article

The IgM receptor FcμR limits tonic BCR signaling by regulating expression of the IgM BCR

MPS-Authors

Kläsener,  Kathrin
External Organizations;
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Zürn,  Christa
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Reth,  Michael
External Organizations;
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Nguyen, T. T. T., Kläsener, K., Zürn, C., Castillo, P. A., Brust-Mascher, I., Imai, D. M., et al. (2017). The IgM receptor FcμR limits tonic BCR signaling by regulating expression of the IgM BCR. Nature Immunology, 18, 321-333. doi:10.1038/ni.3677.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002E-85FE-D
Abstract
The FcμR receptor for the crystallizable fragment (Fc) of immunoglobulin M (IgM) can function as a cell-surface receptor for secreted IgM on a variety of cell types. We found here that FcμR was also expressed in the trans-Golgi network of developing B cells, where it constrained transport of the IgM-isotype BCR (IgM-BCR) but not of the IgD-isotype BCR (IgD-BCR). In the absence of FcμR, the surface expression of IgM-BCR was increased, which resulted in enhanced tonic BCR signaling. B-cell-specific deficiency in FcμR enhanced the spontaneous differentiation of B-1 cells, which resulted in increased serum concentrations of natural IgM and dysregulated homeostasis of B-2 cells; this caused the spontaneous formation of germinal centers, increased titers of serum autoantibodies and excessive accumulation of B cells. Thus, FcμR serves as a critical regulator of B cell biology by constraining the transport and cell-surface expression of IgM-BCR.