6533b837fe1ef96bd12a28ac

RESEARCH PRODUCT

The IgG1 B-cell receptor provides survival and proliferative signals analogue to the Igα but not the Igβ co-receptor.

Ari WaismanJian SongJian SongSabine ClassenNathalie Uyttersprot

subject

0301 basic medicineCo-receptorImmunologyB-cell receptorbcl-X ProteinReceptors Antigen B-CellBiologyCell Line03 medical and health sciencesTransduction (genetics)Mice0302 clinical medicineTranscription (biology)Immunology and AllergyAnimalsCyclin D2TyrosineReceptorCell ProliferationB-Lymphocytesbreakpoint cluster regionFlow CytometryCell biology030104 developmental biologyImmunoglobulin MCytoplasmImmunoglobulin GCancer researchCD79 Antigens030215 immunologySignal Transduction

description

The function of the IgM B-cell receptor (BCR) is dependent on intact signaling of the co-receptors Igα and Igβ, both of which 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 Igα. Here, we show that unlike Igα, Igβ signaling is indispensable for the development and function of IgG1-expressing B cells. Deletion of the cytoplasmic signaling tail of Igβ 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 Igβ, 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 Igα and Igβ in the transduction of IgG1 BCR signal.

10.1002/eji.201646396https://pubmed.ncbi.nlm.nih.gov/27218486