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B8.7 antigen expression on B-CLL cells and its relationship to the LMW-BCGF responsiveness
S Karray1, C Leprince, H Merle-Beral
1Unité INSERM U 131, Clamart, France.
Insights
The B8.7 antigen, an activation marker, is expressed on B lymphocytes in B-cell chronic lymphocytic leukemia (B-CLL) and non-Hodgkin lymphoma (NHL). Its presence is linked to low-molecular-weight B-cell growth factor (LMW-BCGF) responsiveness and proliferation.
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- B-cell chronic lymphocytic leukemia (B-CLL) and non-Hodgkin lymphoma (NHL) are B-cell malignancies.
- B8.7 antigen is an activation marker on B cells, potentially involved in growth factor response.
- Low-molecular-weight B-cell growth factor (LMW-BCGF) stimulates B-cell proliferation.
Purpose of the Study:
- To investigate the expression of B8.7 antigen on malignant B cells from B-CLL and NHL patients.
- To determine the role of B8.7 antigen in LMW-BCGF-induced B-cell proliferation.
- To assess the effect of anti-B8.7 monoclonal antibody (MoAb) on malignant B-cell proliferation.
Main Methods:
- Flow cytometry to detect B8.7 antigen expression on patient-derived B lymphocytes.
- Cell proliferation assays assessing DNA synthesis induced by LMW-BCGF.
- Inhibition studies using anti-B8.7 MoAb to block LMW-BCGF-dependent proliferation.
Main Results:
- B8.7 antigen was expressed on B lymphocytes from 11 of 22 B-CLL patients.
- LMW-BCGF induced DNA synthesis in B8.7-positive malignant B cells, often without anti-mu antibody costimulation.
- Anti-B8.7 MoAb inhibited LMW-BCGF-dependent proliferation of these malignant B cells, similar to normal B cells.
Conclusions:
- The B8.7 molecule is expressed on malignant B cells in B-CLL and NHL.
- B8.7 antigen plays a role in the signaling pathway of LMW-BCGF.
- Targeting B8.7 may offer a therapeutic strategy for B-cell malignancies by inhibiting LMW-BCGF-driven proliferation.
Abstract:
In this work, we studied the expression of B8.7 antigen on B lymphocytes from patients suffering from B type chronic lymphocytic leukemia (B-CLL) as well as on non Hodgkin lymphoma cells (NHL). B8.7 is an activation marker, which has been reported to be associated with the capacity of activated B cells to respond to LMW-BCGF. B lymphocytes of 11 out of 22 patients tested were B8.7 positive. With the exception of one case, LMW-BCGF is able to induce DNA synthesis by these cells in the absence of costimulation by anti-mu antibodies (anti-mu Ab). The LMW-BCGF dependent proliferation of these malignant cells is inhibited by the anti-B8.7 monoclonal antibody (anti-B8.7 MoAb), in the same line as that of normal B cells. These results obtained with monoclonal B cells confirm that the B8.7 molecule is involved in the signalling pathway of the LMW-BCGF.