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Updated: May 21, 2026

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Chronic lymphocytic leukemia and regulatory B cells share IL-10 competence and immunosuppressive function
D J DiLillo1, J B Weinberg, A Yoshizaki
1Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA.
Insights
Chronic lymphocytic leukemia (CLL) cells produce interleukin-10 (IL-10), similar to regulatory B10 cells. These IL-10-producing CLL cells may contribute to the immunosuppression seen in patients.
Area of Science:
- Immunology
- Hematology
- Oncology
Background:
- Chronic lymphocytic leukemia (CLL) is associated with immunosuppression.
- CLL cells share markers with regulatory B cells (B10 cells) that produce interleukin-10 (IL-10).
Purpose of the Study:
- To investigate the functional links between CLL cells and regulatory B10 cells.
- To assess the IL-10 production capacity of leukemia cells in CLL patients.
Main Methods:
- Phenotypic analysis and IL-10 expression assessment of leukemia cells from 93 CLL patients.
- Evaluation of IL-10 levels in patient serum.
- Analysis of IL-10-competent B cells in TCL1-transgenic mouse models of CLL.
Main Results:
- CD5(+) CLL cells from 90% of patients were IL-10-competent and secreted IL-10 upon stimulation.
- Elevated serum IL-10 levels were observed in CLL patients.
- IL-10-competent B cells expanded in TCL1-Tg mice, preceding leukemia development, and malignant CLL cells exhibited regulatory functions.
Conclusions:
- Malignant CLL cells are IL-10-competent and possess regulatory functions akin to B10 cells.
- IL-10 production by CLL cells may contribute to immunosuppression in CLL patients and mouse models.
Abstract:
Chronic lymphocytic leukemia (CLL) can be immunosuppressive in humans and mice, and CLL cells share multiple phenotypic markers with regulatory B cells that are competent to produce interleukin (IL)-10 (B10 cells). To identify functional links between CLL cells and regulatory B10 cells, the phenotypes and abilities of leukemia cells from 93 patients with overt CLL to express IL-10 were assessed. CD5(+) CLL cells purified from 90% of the patients were IL-10-competent and secreted IL-10 following appropriate ex vivo stimulation. Serum IL-10 levels were also significantly elevated in CLL patients. IL-10-competent cell frequencies were higher among CLLs with IgV(H) mutations, and correlated positively with TCL1 expression. In the TCL1-transgenic (TCL1-Tg) mouse model of CLL, IL-10-competent B cells with the cell surface phenotype of B10 cells expanded significantly with age, preceding the development of overt, CLL-like leukemia. Malignant CLL cells in TCL1-Tg mice also shared immunoregulatory functions with mouse and human B10 cells. Serum IL-10 levels varied in TCL1-Tg mice, but in vivo low-dose lipopolysaccharide treatment induced IL-10 expression in CLL cells and high levels of serum IL-10. Thus, malignant IL-10-competent CLL cells exhibit regulatory functions comparable to normal B10 cells that may contribute to the immunosuppression observed in patients and TCL1-Tg mice.
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