Involvement of IL‑10 and granulocyte colony‑stimulating factor in the fate of monocytes controlled by galectin‑1
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Updated: Apr 23, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Da-En Cheng1, Wei-An Chang2, Jen-Yu Hung3
1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan, R.O.C.
Abstract:
The process of differentiation from monocytes to dendritic cells is critical in immune modulation. Monocyte apoptosis is a key regulator in balancing the immune response. Galectin‑1 has been reported to induce tolerogenic dendritic cells by the autocrine interleukin (IL)‑10 in monocytes. However, IL‑10 has been found to induce apoptosis in IL‑4/granulocyte macrophage colony‑stimulating factor (CSF) stimulating and non‑stimulating monocytes, whereas galectin‑1 has not. After analyzing the factors secreted by galectin-1-activated CD14 monocytes isolated from the peripheral blood, the present study revealed that galectin‑1 upregulates IL‑10 and granulocyte (G)-CSF expression. Furthermore, G‑CSF inhibited IL‑10‑induced apoptosis, implying that galectin‑1 may enhance the immune‑modulating functions of G‑CSF by inducing tolerogenic dendritic cells and maintaining their survival. Therefore, G‑CSF may be further applied in immune therapy, particularly in the IL‑10‑presenting microenvironment.
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