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Published on: November 26, 2018
Immunomodulatory effects of galectin-1 in patients with chronic lymphocytic leukemia
Milos Kostic1, Tanja Dzopalic1, Goran Marjanovic1,2
1Department of Immunology, Medical Faculty of Nis, University of Nis, Nis, Serbia.
Insights
Galectin-1 in chronic lymphocytic leukemia (CLL) serum drives immunodeficiency by increasing IL-10. Inhibiting Galectin-1 (Gal-1) with OTX008 reduced IL-10, suggesting a therapeutic target for CLL-associated immune dysfunction.
Area of Science:
- Immunology
- Hematology
- Cancer Biology
Background:
- Chronic lymphocytic leukemia (CLL) is often associated with immunodeficiency.
- Galectin-1 (Gal-1) is implicated in CLL progression and immune dysfunction.
Purpose of the Study:
- To investigate the impact of Gal-1 inhibition on dendritic cell (DC) immunomodulatory properties in CLL patients.
- To explore the role of Gal-1 in serum from immunocompromised CLL patients.
Main Methods:
- Dendritic cells (DCs) were derived from peripheral blood mononuclear cells.
- DCs were treated with healthy serum, CLL serum, or CLL serum with a Gal-1 inhibitor (OTX008).
- DC maturation markers, cytokine profiles, and T cell polarization were analyzed.
Main Results:
- CLL serum increased interleukin-10 (IL-10) production in DCs and CD4+ T cells.
- OTX008 treatment reduced IL-10 and IL-2 production.
- No significant changes in DC maturation markers or regulatory T cell frequency were observed.
Conclusions:
- Gal-1 in CLL serum induces a specific IL-10+ CD4+ T cell phenotype, distinct from regulatory T cells.
- This Gal-1-driven T cell response may contribute to the immunodeficiency observed in CLL patients.
- Targeting Gal-1 may offer a strategy to restore immune function in CLL.
Abstract:
Galectin-1 (Gal-1) has been implicated in the progression of chronic lymphocytic leukemia (CLL) but also the development of immunodeficiency, which commonly accompany this malignancy. In this in vitro study, we investigated the effects of Gal-1 inhibition in the sera of immunocompromised CLL patients on immunomodulating properties of dendritic cells (DCs). DCs derived from peripheral blood mononuclear cells were treated with a healthy serum, CLL serum as well as the combination of CLL serum and Gal-1 inhibitor (OTX008). Following the treatment, the expression levels of DC maturation markers (CD80, CD83, CD86 and IDO-1) were determined as well as their cytokine profile and the ability to polarize the immune response in co-cultures with CD4+ T cells. After treatment with CLL serum, an increase in interleukin (IL)-10 production was observed in both DC cultures and co-cultures with CD4+ T cells. OTX008 caused a reduction in IL-10 production as well as IL-2, but no significant alteration in the expression of DC maturation markers or T regulatory cell (Treg) frequency was observed. The results of our study suggest that Gal-1 from CLL serum give rise to a specific IL-10+ CD4+ T cell phenotype, other than Treg, that could mediate immunodeficiency development in CLL patients.
