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© Andres Alcover
Scanning electron microscopy showing a conjugate formed between a T lymphocyte and an antigen presenting cell. It is worth noting the long shape of the T cell (Tc) polarized towards the antigen presenting cell (APC) and the membrane protrusions that adhere the T lymphocyte to the antigen presenting cell.
Publication : British journal of haematology

Defective assembly of the B-cell receptor chains accounts for its low expression in B-chronic lymphocytic leukaemia

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in British journal of haematology - 01 Sep 2002

Payelle-Brogard B, Magnac C, Alcover A, Roux P, Dighiero G

Link to Pubmed [PMID] – 12199775

Br. J. Haematol. 2002 Sep;118(4):976-85

B-cell chronic lymphocytic leukaemia (B-CLL) characteristically displays low amounts of B-cell receptor (BCR), which mainly consists of the heterodimer CD79a/CD79b bound non-covalently with the surface immunoglobulin (SIg). This heterodimer is required for SIg expression and BCR signalling. To better define the mechanisms related to low BCR expression, we have investigated transcription, protein synthesis, assembly and transport of the BCR in B-CLL cells. Our results demonstrated that: (1) there was no major defect in transcriptional expression of the B29 (CD79b) gene; (2) the BCR components were intracellularly detected, thus adequately synthesized, in almost all patients; (3) neither a genetic defect in the transmembrane region of SIg, which associated with CD79a/CD79b, nor a genetic abnormality in the chaperone protein calnexin that is involved in folding and assembly of the BCR were found; (4) a constant defect in the assembly of IgM and CD79b chains occurred leading to abnormal accumulation of both chains in different intracellular compartments; (5) in a majority of CLL patients all of the nascent IgM failed to be processed into mature chains and remained unsuitable for transport. These findings demonstrated that a post-transcriptional defect located at the BCR intracellular assembly and/or trafficking levels could be involved in its low surface expression in B-CLL.

https://www.ncbi.nlm.nih.gov/pubmed/12199775