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Heterogeneous intracellular expression of B‐cell receptor components in B‐cell chronic lymphocytic leukaemia (B‐CLL) cells and effects of CD79b gene transfer on surface immunoglobulin levels in a B‐CLL‐derived cell line
Author(s) -
Minuzzo Sonia,
Indraccolo Stefano,
Tosello Valeria,
Piovan Erich,
Cabrelle Anna,
Trentin Livio,
Semenzato Giampietro,
Amadori Alberto
Publication year - 2005
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2005.05699.x
Subject(s) - intracellular , breakpoint cluster region , b cell , b cell receptor , antibody , flow cytometry , chronic lymphocytic leukemia , transfection , immunology , cell , cell culture , cancer research , biology , medicine , receptor , microbiology and biotechnology , leukemia , genetics
Summary B‐cell chronic lymphocytic leukaemia (B‐CLL) cells display low amounts of surface immunoglobulins (sIg). To investigate the mechanisms underlying this phenomenon, we performed a thorough study of surface and intracellular expression of the B‐cell receptor (BCR) components in B‐CLL cells using flow cytometry. There was an heterogeneous pattern of expression. Overall, 20 of 22 samples showed reduced sIgM levels, compared with normal B cells. Among them, three (15%) had very low to undetectable intracellular IgM levels and variable amounts of CD79a and CD79b; nine (45%) had low intracellular CD79b levels but appreciable levels of IgM and CD79a; and eight (40%) had relatively normal intracellular levels of all BCR components. To investigate whether surface BCR levels could be controlled by the rate of CD79b synthesis, adenoviral vectors encoding CD79b were generated and used for gene transfer experiments. Delivery of CD79b to non‐B cells transfected with IgM and CD79a lead to high‐level expression of a functional BCR. Moreover, CD79b gene transfer in a B cell line derived from a B‐CLL patient and characterised by low intracellular levels of endogenous CD79b consistently increased sIgM levels. These findings indicate that the phenotype of B‐CLL cells in a subset of patients may depend primarily on poor CD79b expression, and suggest that upregulation of CD79b expression may correct the phenotype of these cells.