Expression of the T-cell-specific tyrosine kinase Lck in normal B-1 cells and in chronic lymphocytic leukemia B cells

• Published in: Blood 1998-05, Vol.91 (9), p.3390-3396
• Main Authors: MAJOLINI, M. B, D'ELIOS, M. M, GALIENI, P, BONCRISTIANO, M, LAURIA, F, DEL PRETE, G, TELFORD, J. L, BALDARI, C. T
• Format: Article
• Language: English
• Subjects: B-Lymphocyte Subsets - enzymology; Biological and medical sciences; Blotting, Western; CD5 Antigens - analysis; Cell Transformation, Viral; Hematologic and hematopoietic diseases; Herpesvirus 4, Human; Humans; Leukemia, Lymphocytic, Chronic, B-Cell - enzymology; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - metabolism; Medical sciences; Phosphopyruvate Hydratase - metabolism; Phosphorylation; RNA, Messenger - genetics; RNA, Neoplasm - genetics; T-Lymphocytes - enzymology; Tumor Cells, Cultured - enzymology
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.v91.9.3390

Src family kinases play a key role in mitogenesis. The exquisitely tissue-specific distribution of different Src family members suggests that a fine tuning of their expression might be a key prerequisite for cell homeostasis. We tested B cells from patients affected by B-cell chronic lymphocytic leukemia (B-CLL) for expression of Src family kinases. The T-cell-specific tyrosine kinase Lck was found to be expressed at significant levels in CLL B-cells. This finding could be accounted for either by ectopic expression of Lck in B-CLL or by specific expression of this kinase in normal B-1 cells, which are believed to be the normal counterpart of CLL B cells. To answer this question B cells from different sources, characterized by a different size of the B-1 subpopulation, were tested for Lck expression. The results show that Lck expression is a feature of CD5(+), B-1 cells, suggesting a potential role for Lck in the self-renewal capacity of this B-cell subpopulation and supporting the notion that B-1 cells are the subset undergoing oncogenic transformation in B-CLL. Furthermore, we show that the CD5(-), B-2 subpopulation, while normally lacking Lck expression, acquires the capacity to express Lck ectopically upon transformation by EBV.