Phenotypic heterogeneity of B cell chronic lymphocytic leukaemia
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1Department of Haematology, Riga Medical Institute, Latvian, U.S.S.R.
Insights
This study identified two distinct B cell phenotypes in chronic lymphocytic leukemia (CLL) patients. One group showed low surface immunoglobulin density, while the other co-expressed CD22, CD21, and CD35, crucial for B cell activation.
Area of Science:
- Hematology
- Immunology
- Oncology
Background:
- Chronic lymphocytic leukemia (CLL) is a B cell malignancy.
- Phenotypic characterization of CLL cells is crucial for understanding disease heterogeneity.
Purpose of the Study:
- To investigate the immunophenotypic profiles of B cells in CLL patients.
- To identify distinct CLL patient groups based on cell surface marker expression.
Main Methods:
- Peripheral blood lymphocytes from 39 CLL patients were analyzed.
- Monoclonal antibodies targeting various clusters of differentiation (CD) were used for phenotyping.
- Flow cytometry and microscopy were employed for cell analysis.
Main Results:
- Two distinct patient groups were identified based on CD marker expression.
- The major group (33/39) exhibited low surface immunoglobulin density and lacked CD21, CD22, and CD35.
- A smaller group (6/39) showed co-expression of CD22, CD21 (CR2), and CD35 (CR1).
Conclusions:
- Distinct immunophenotypic profiles exist within CLL patient populations.
- The co-expression of CD22, CD21, and CD35 in a subset of CLL patients may indicate specific B cell activation pathways.
- Further research is needed to correlate these findings with clinical outcomes.
Abstract:
The peripheral blood lymphocytes from 39 patients from the Latvian S.S.R.T., U.S.S.R. with chronic lymphocytic leukaemia (CLL) have been phenotyped with various monoclonal antibodies representing the major clusters of differentiation (CD) used for phenotyping B cells. A clear delineation of two groups of patients was evidenced. The major group (33/39) possessed leukaemic cells bearing surface immunoglobulins (SIg) at a low density, Class II HLA, and CD5, CD24 and CD37 molecules but not CD21, CD22 and CD35. CD23 antigen was seen only once under microscope examination, but could be visualized by flow cytometry. CD6 antibody reacted with cells from about 1/3 of this group of patients. In the six patients of the second group the leukaemic phenotype was SIg+, Class II HLA+, CD5+, 24+, 37+, 21+, 22+, 35+, 23+ and 6-. The main finding is the concomitant expression of CD22, CD21 (CR2) and CD35 (CR1) molecules, all involved in B cell activation. It is not yet known whether these observations correlate with different clinical evolutions of the disease.
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