Galectin-3 regulates the innate immune response of human monocytes

Andrew W. Chung; Peter A. Sieling; Mirjam Schenk; Rosane M B Teles; Stephan R. Krutzik; Daniel K. Hsu; Fu-Tong Liu; Euzenir N. Sarno; Thomas H. Rea; Steffen Stenger; Robert L. Modlin; Delphine J. Lee

doi:10.1093/infdis/jis920

Galectin-3 regulates the innate immune response of human monocytes

Andrew W. Chung, Peter A. Sieling, Mirjam Schenk, Rosane M B Teles, Stephan R. Krutzik, Daniel K. Hsu, Fu-Tong Liu, Euzenir N. Sarno, Thomas H. Rea, Steffen Stenger, Robert L. Modlin, Delphine J. Lee

Dermatology

Research output: Contribution to journal › Article

18 Scopus citations

Abstract

Galectin-3 is a β-galactoside-binding lectin widely expressed on epithelial and hematopoietic cells, and its expression is frequently associated with a poor prognosis in cancer. Because it has not been well-studied in human infectious disease, we examined galectin-3 expression in mycobacterial infection by studying leprosy, an intracellular infection caused by Mycobacterium leprae. Galectin-3 was highly expressed on macrophages in lesions of patients with the clinically progressive lepromatous form of leprosy; in contrast, galectin-3 was almost undetectable in self-limited tuberculoid lesions. We investigated the potential function of galectin-3 in cell-mediated immunity using peripheral blood monocytes. Galectin-3 enhanced monocyte interleukin 10 production to a TLR2/1 ligand, whereas interleukin 12p40 secretion was unaffected. Furthermore, galectin-3 diminished monocyte to dendritic cell differentiation and T-cell antigen presentation. These data demonstrate an association of galectin-3 with unfavorable host response in leprosy and a potential mechanism for impaired host defense in humans.

Original language	English (US)
Pages (from-to)	947-956
Number of pages	10
Journal	Journal of Infectious Diseases
Volume	207
Issue number	6
DOIs	https://doi.org/10.1093/infdis/jis920
State	Published - 2013

Keywords

bacterial infections
galectin-3
human
monocytes/macrophages
TLR2

ASJC Scopus subject areas

Infectious Diseases
Immunology and Allergy

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10.1093/infdis/jis920

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Chung, A. W., Sieling, P. A., Schenk, M., Teles, R. M. B., Krutzik, S. R., Hsu, D. K., Liu, F-T., Sarno, E. N., Rea, T. H., Stenger, S., Modlin, R. L., & Lee, D. J. (2013). Galectin-3 regulates the innate immune response of human monocytes. Journal of Infectious Diseases, 207(6), 947-956. https://doi.org/10.1093/infdis/jis920

Galectin-3 regulates the innate immune response of human monocytes. / Chung, Andrew W.; Sieling, Peter A.; Schenk, Mirjam; Teles, Rosane M B; Krutzik, Stephan R.; Hsu, Daniel K.; Liu, Fu-Tong; Sarno, Euzenir N.; Rea, Thomas H.; Stenger, Steffen; Modlin, Robert L.; Lee, Delphine J.

In: Journal of Infectious Diseases, Vol. 207, No. 6, 2013, p. 947-956.

Research output: Contribution to journal › Article

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abstract = "Galectin-3 is a β-galactoside-binding lectin widely expressed on epithelial and hematopoietic cells, and its expression is frequently associated with a poor prognosis in cancer. Because it has not been well-studied in human infectious disease, we examined galectin-3 expression in mycobacterial infection by studying leprosy, an intracellular infection caused by Mycobacterium leprae. Galectin-3 was highly expressed on macrophages in lesions of patients with the clinically progressive lepromatous form of leprosy; in contrast, galectin-3 was almost undetectable in self-limited tuberculoid lesions. We investigated the potential function of galectin-3 in cell-mediated immunity using peripheral blood monocytes. Galectin-3 enhanced monocyte interleukin 10 production to a TLR2/1 ligand, whereas interleukin 12p40 secretion was unaffected. Furthermore, galectin-3 diminished monocyte to dendritic cell differentiation and T-cell antigen presentation. These data demonstrate an association of galectin-3 with unfavorable host response in leprosy and a potential mechanism for impaired host defense in humans.",

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AB - Galectin-3 is a β-galactoside-binding lectin widely expressed on epithelial and hematopoietic cells, and its expression is frequently associated with a poor prognosis in cancer. Because it has not been well-studied in human infectious disease, we examined galectin-3 expression in mycobacterial infection by studying leprosy, an intracellular infection caused by Mycobacterium leprae. Galectin-3 was highly expressed on macrophages in lesions of patients with the clinically progressive lepromatous form of leprosy; in contrast, galectin-3 was almost undetectable in self-limited tuberculoid lesions. We investigated the potential function of galectin-3 in cell-mediated immunity using peripheral blood monocytes. Galectin-3 enhanced monocyte interleukin 10 production to a TLR2/1 ligand, whereas interleukin 12p40 secretion was unaffected. Furthermore, galectin-3 diminished monocyte to dendritic cell differentiation and T-cell antigen presentation. These data demonstrate an association of galectin-3 with unfavorable host response in leprosy and a potential mechanism for impaired host defense in humans.

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