Song, Jian ORCID: 0000-0002-2459-7046, Uyttersprot, Nathalie, Classen, Sabine and Waisman, Ari ORCID: 0000-0003-4304-8234 (2016). The IgG1 B-cell receptor provides survival and proliferative signals analogue to the Ig alpha but not the Ig beta co-receptor. Eur. J. Immunol., 46 (8). S. 1878 - 1887. HOBOKEN: WILEY-BLACKWELL. ISSN 1521-4141

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Abstract

The function of the IgM B-cell receptor (BCR) is dependent on intact signaling of the co-receptors Ig alpha and Ig beta, both ofwhich contain a cytoplasmic tail bearing an immunoreceptor tyrosine-based activation motif. We have previously demonstrated that the cytoplasmic tail of the IgG1 BCR can partially compensate for the loss of the signaling moiety of Ig alpha. Here, we show that unlike Ig alpha, Ig beta signaling is indispensable for the development and function of IgG1-expressing B cells. Deletion of the cytoplasmic signaling tail of Ig beta compromised the survival and proliferation not only of IgM(+) B cells but also of IgG1-expressing B cells. In the absence of the signaling tail of Ig beta, the transcription levels of the antiapoptotic gene bcl-xl and the cell-cycle gene ccnd2 were reduced, consistent with the observed defects in survival and proliferation. These results demonstrate functional differences between Ig alpha and Ig beta in the transduction of IgG1 BCR signal.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Song, JianUNSPECIFIEDorcid.org/0000-0002-2459-7046UNSPECIFIED
Uyttersprot, NathalieUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Classen, SabineUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Waisman, AriUNSPECIFIEDorcid.org/0000-0003-4304-8234UNSPECIFIED
URN: urn:nbn:de:hbz:38-267423
DOI: 10.1002/eji.201646396
Journal or Publication Title: Eur. J. Immunol.
Volume: 46
Number: 8
Page Range: S. 1878 - 1887
Date: 2016
Publisher: WILEY-BLACKWELL
Place of Publication: HOBOKEN
ISSN: 1521-4141
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
ANTIGEN RECEPTOR; LYMPHOCYTES; TOLERANCE; CD22; MICE; TAILMultiple languages
ImmunologyMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/26742

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