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Changes in adhesion molecule expression and function in B-cell chronic lymphocytic leukaemia after in vitro
G Csanaky1, J A Vass, I Ocsovszki
1Department of Pathology, University Medical School of Pécs, Hungary.
European Journal of Haematology
|January 1, 1995
Summary
Interferon-alpha (IFN-alpha) stimulation increases L-selectin expression and function on B-cell chronic lymphocytic leukemia (B-CLL) cells. This enhanced function may explain IFN-alpha
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- B-cell chronic lymphocytic leukemia (B-CLL) is characterized by the accumulation of leukemic B cells.
- Adhesion molecules play a crucial role in cell trafficking and interactions.
- Interferon-alpha (IFN-alpha) is used therapeutically for B-CLL, but its mechanism of action requires further elucidation.
Purpose of the Study:
- To investigate the expression and function of adhesion molecules on B-CLL cells following in vitro IFN-alpha stimulation.
- To compare IFN-alpha-induced changes with established assays for cell adhesion.
Main Methods:
- Peripheral blood mononuclear cells (PBMCs) from 10 B-CLL patients were stimulated with IFN-alpha for 24 hours.
- Expression of L-selectins (LECAM-1), LFA-1/CD11a, VLA alpha-4/CDw49d, and ICAM-1/CD54 was analyzed.
- Functional assays included high endothelial venule (HEV)-binding and carbohydrate (PPME, fucoidin) immobilization tests.
Main Results:
- LECAM-1 and ICAM-1 were highly expressed on most CLL cells; LFA-1 and VLA-4 were expressed by fewer cells.
- IFN-alpha stimulation significantly increased LECAM-1 antigen density (p < 0.001) and enhanced HEV-, PPME-, and fucoidin-binding (p < 0.01).
- These findings suggest enhanced L-selectin expression and function post-IFN-alpha treatment.
Conclusions:
- IFN-alpha stimulation upregulates both the expression and function of L-selectins on B-CLL cells.
- The enhanced L-selectin function may contribute to the therapeutic efficacy of IFN-alpha in reducing leukemic cell accumulation.
- Further research is needed to clarify the role of ICAM-1 in B-CLL.