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

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.

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https://www.nature.com/articles/ni.3677 (Verlagsversion)
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 Urheber:
Nguyen, Trang T T1, Autor
Kläsener, Kathrin1, 2, Autor
Zürn, Christa2, Autor
Castillo, Patricia A1, Autor
Brust-Mascher, Ingrid1, Autor
Imai, Denise M1, Autor
Bevins, Charles L1, Autor
Reardon, Colin1, Autor
Reth, Michael 1, 2, Autor
Baumgarth, Nicole1, Autor
Affiliations:
1External Organizations, ou_persistent22              
2Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, 79108 Freiburg, DE, ou_2243645              

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 Zusammenfassung: 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.

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Sprache(n): eng - English
 Datum: 2017-03
 Publikationsstatus: Erschienen
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 Ort, Verlag, Ausgabe: -
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 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1038/ni.3677
 Art des Abschluß: -

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Titel: Nature Immunology
  Andere : Nat. Immunol.
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: New York, NY : Nature America Inc.
Seiten: - Band / Heft: 18 Artikelnummer: - Start- / Endseite: 321 - 333 Identifikator: ISSN: 1529-2908
CoNE: https://pure.mpg.de/cone/journals/resource/974392607073