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Published on: October 19, 2014
[Defective expression of B7.2 in B cell chronic lymphocytic leukemia B cells]
1Department of Hematology, Affiliated Huashan Hospital, Fudan University Medical School, Shanghai 200040, China.
Insights
B7.2 molecule expression is defective in chronic B cell lymphocytic leukemia (BCLL) patients, potentially hindering immune clearance of BCLL cells. This defect in B7.2 expression may contribute to BCLL pathogenesis.
Area of Science:
- Immunology
- Hematology
- Oncology
Background:
- Chronic B cell lymphocytic leukemia (BCLL) is a malignancy characterized by the accumulation of malignant B lymphocytes.
- The B7 family of molecules, including B7.1 and B7.2, play crucial roles in T cell activation and immune regulation.
- Dysregulation of co-stimulatory molecules can contribute to immune evasion in various cancers.
Purpose of the Study:
- To investigate the expression levels of B7.1 and B7.2 molecules on peripheral B cells in patients with BCLL.
- To explore the correlation between B7.1 and B7.2 expression and the underlying pathogenic mechanisms of BCLL.
- To determine if B7.1 and B7.2 expression differs between early and advanced stages of BCLL.
Main Methods:
- Peripheral blood mononuclear cells (PBMC) were isolated from 23 BCLL patients and 25 healthy controls.
- Flow cytometry (FCM) was employed to analyze B7.1 and B7.2 expression on peripheral B cells after 24 hours of in vitro culture.
- BCLL patients were stratified into early (phase 0-II) and advanced (phase III-IV) disease groups.
Main Results:
- Significantly lower B7.2 expression was observed in B cells of BCLL patients compared to healthy controls (P < 0.05).
- No significant differences in B7.1 expression or co-expression of B7.1 and B7.2 were found between BCLL patients and controls.
- Average B7.2 expression rates in early and advanced BCLL stages were 25% +/- 17% and 17% +/- 8%, respectively, with no statistically significant difference between stages.
Conclusions:
- Defective B7.2 expression in BCLL B cells is identified as a potential pathogenic mechanism.
- This B7.2 deficiency may impair the body's ability to eliminate BCLL cells through immunological responses.
- Targeting B7.2 expression could be a potential therapeutic strategy for BCLL.
Objective:
To investigate the expression of B7.1 and B7.2 molecules in peripheral B cells of patients with chronic B cell lymphocytic leukemia (BCLL) and to study the relationship between B7.1 and B7.2 expression and pathogenic mechanism of BCLL.
Methods:
Peripheral blood mononuclear cells (PBMC) were separated by Ficoll-Hypaque lymphocytes separation medium from 25 normal persons (normal control group) and 23 BCLL patients (BCLL group) which were further divided into two groups, phase 0-II group and phase III-IV group. Flow cytometry (FCM) was used to analyze the B7.1 and B7.2 expression in peripheral B cells after the mononuclear cells had been cultured for 24 hours in vitro.
Results:
The B7.2 expression in B cells of BCLL patients was significantly lower than that in normal control group (P < 0.05). No statistically significant difference was found in the B7.1 expression and co-expression of B7.1 and B7.2 between the BCLL group and normal control group. The average B7.2 expression rates in patients of phase 0-II group and phase III-IV group were 25% +/- 17% and 17% +/- 8% respectively without statistically significant difference.
Conclusion:
The B7.2 expression in B cell of patients with BCLL is defective, which may be one of the pathogenic mechanisms of chronic BCLL and a major cause why the body fails to clear the BCLL cells via immunological means.
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