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Differential adhesion pattern of B cell chronic lymphocytic leukemia cells
S I Behr1, D Korinth, F Schriever
1Department of Hematology and Oncology, Virchow University Hospital, Humboldt Universität Berlin, Germany.
Leukemia
|January 22, 1998
Summary
B cell chronic lymphocytic leukemia (B-CLL) cells bind to lymphoid tissues via specific adhesion molecules. CD19 antibodies trigger B-CLL cell clumping, suggesting these interactions facilitate B-CLL cell migration in the body.
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- Cellular adhesion and migration are critical in B cell chronic lymphocytic leukemia (B-CLL) pathophysiology.
- The precise adhesion pathways governing B-CLL cell trafficking and intercellular adhesion remain unclear.
Purpose of the Study:
- To identify mechanisms of B-CLL cell binding to secondary lymphoid organs.
- To elucidate mechanisms of homotypic B-CLL cell aggregation.
Main Methods:
- Investigated B-CLL cell binding to human tonsils in situ.
- Utilized monoclonal antibodies (mAbs) to study homotypic B-CLL cell aggregation.
- Assessed the role of protein synthesis in anti-CD19-induced aggregation.
Main Results:
- B-CLL cells adhered to tonsil germinal centers via integrin alpha4beta1/vascular cell adhesion molecule-1 (VCAM-1).
- Monoclonal antibodies against CD19 induced B-CLL cell aggregation through integrin alphaL (leukocyte function antigen-1 (LFA-1)), intercellular adhesion molecule-1 (ICAM-1), and CD21.
- CD19-induced aggregation was dependent on protein synthesis.
Conclusions:
- Integrin alpha4beta1/VCAM-1 mediates B-CLL cell binding to lymphoid tissues.
- CD19 signaling induces homotypic B-CLL cell adhesion via LFA-1, ICAM-1, and CD21, requiring protein synthesis.
- These adhesion mechanisms likely contribute to B-CLL cell migration in vivo.