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 (2013). Galectin-3 regulates the innate immune response of human monocytes. Journal of infectious diseases, 207(6), pp. 947-956. Oxford University Press 10.1093/infdis/jis920

[img] Text
23255567.pdf - Published Version
Restricted to registered users only
Available under License Publisher holds Copyright.

Download (8MB) | Request a copy

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.

Item Type:

Journal Article (Original Article)


04 Faculty of Medicine > Service Sector > Institute of Pathology > Immunopathology

UniBE Contributor:

Schenk, Mirjam




Oxford University Press




Mirjam Schenk

Date Deposited:

25 Jul 2017 15:36

Last Modified:

05 Dec 2022 15:06

Publisher DOI:


PubMed ID:





Actions (login required)

Edit item Edit item
Provide Feedback