English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Responsiveness of B cell is regulated by hinge region of IgD

MPS-Authors

Kometani,  Kohei
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191285

Reth,  Michael
BIOSS Center for Biological Signaling Studies, Albert-Ludwigs University of Freiburg;
Department of Molecular Immunology, Biology III, Faculty of Biology, Albert-Ludwigs University of Freiburg;
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Übelhart, R., Hug, E., Bach, M. P., Wossning, T., Dühren-von Minden, M., Horn, A. H., et al. (2015). Responsiveness of B cell is regulated by hinge region of IgD. Nature Immunology, 16, 534-543. doi:doi: 10.1038/ni.3141.


Cite as: https://hdl.handle.net/someHandle/test/escidoc:902688
Abstract
Mature B cells express immunoglobulin M (IgM)- and IgD-isotype B cell antigen receptors, but the importance of IgD for B cell function has been unclear. By using a cellular in vitro system and corresponding mouse models, we found that antigens with low valence activated IgM receptors but failed to trigger IgD signaling, whereas polyvalent antigens activated both receptor types. Investigations of the molecular mechanism showed that deletion of the IgD-specific hinge region rendered IgD responsive to monovalent antigen, whereas transferring the hinge to IgM resulted in responsiveness only to polyvalent antigen. Our data suggest that the increased IgD/IgM ratio on conventional B-2 cells is important for preferential immune responses to antigens in immune complexes, and that the increased IgM expression on B-1 cells is essential for B-1 cell homeostasis and function.