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GALECTIN-3 REGULATES THE INNATE IMMUNE RESPONSE OF HUMAN MONOCYTES
Chung, Andrew W. et al. | Date Issued: 2013
Author
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.
Affilliation
John Wayne Cancer Institute at Saint John’s Health Center. Department of Translational Immunology. 1Dirks/Dougherty Laboratory for Cancer Research. Santa Monica, CA, USA.
John Wayne Cancer Institute at Saint John’s Health Center. Department of Translational Immunology. 1Dirks/Dougherty Laboratory for Cancer Research. Santa Monica, CA, USA.
University of California. David Geffen School of Medicine. Department of Medicine. Division of Dermatology. Los Angeles, USA.
University of California. David Geffen School of Medicine. Department of Medicine. Division of Dermatology. Los Angeles, USA / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.
University of California. David Geffen School of Medicine. Department of Medicine. Division of Dermatology. Los Angeles, USA.
University of California. Davis School of Medicine. Department of Dermatology. Sacramento, USA / Academia Sinica. Institute of BioMedical Sciences. Taipei, Taiwan, Republic of China.
University of California. Davis School of Medicine. Department of Dermatology. Sacramento, USA / Academia Sinica. Institute of BioMedical Sciences. Taipei, Taiwan, Republic of China.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.
University of Southern California. School of Medicine. Department of Dermatology. Los Angeles, USA.
University Hospital of Ulm. Institute for Medical Microbiology and Hygiene. Germany.
University of California. David Geffen School of Medicine. Department of Medicine. Division of Dermatology. Los Angeles, USA / University of California. David Geffen School of Medicine. Department of Microbiology, Immunology, and Molecular Genetics. Los Angeles, USA.
John Wayne Cancer Institute at Saint John’s Health Center. Department of Translational Immunology. 1Dirks/Dougherty Laboratory for Cancer Research. Santa Monica, CA, USA.
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.
Keywords
Human
Bacterial infection
Galectin-3
Monocytes/macrophages;
TLR2
 
DeCS
nfecções Bacterianas
Monócitos
Macrófagos
Humanos
 
Publisher
Oxford University Press
Citation
CHUNG, Andrew W.; et al. Galectin-3 Regulates the Innate Immune Response of Human Monocytes. J. Infect Dis., v.207, n.6, p.947-956, 2013.
DOI
10.1093/infdis/jis920
ISSN
0022-1899
1537-6613