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Mol Med Rep. 2014 Nov;10(5):2389-94. doi: 10.3892/mmr.2014.2573. Epub 2014 Sep 16.

Involvement of IL‑10 and granulocyte colony‑stimulating factor in the fate of monocytes controlled by galectin‑1.

Author information

1
Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan, R.O.C.
2
Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan, R.O.C.
3
Division of Pulmonary and Critical Care Medicine, Kaohsiung Medical University Hospital, 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.

PMID:
25231117
DOI:
10.3892/mmr.2014.2573
[Indexed for MEDLINE]

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