@article{23897,
  keywords = {Antigen Presentation, Antigens, CD1, Cell Differentiation, Galectin 3, Gene Expression, Humans, Immunity, Cellular, Immunity, Innate, Interleukin-10, Interleukin-12 Subunit p40, Leprosy, lepromatous, Leprosy, Tuberculoid, Macrophages, Monocytes, Mycobacterium leprae, RNA, Messenger},
  author = {Chung A and Sieling PA and Schenk M and Teles R and Krutzik SR and Hsu D and Liu F and Sarno E and Rea T and Stenger S and Modlin RL and Lee DJ},
  title = {Galectin-3 regulates the innate immune response of human monocytes.},
  abstract = {<p>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.</p>},
  year = {2013},
  journal = {The Journal of infectious diseases},
  volume = {207},
  pages = {947-56},
  month = {2013 Mar 15},
  issn = {1537-6613},
  doi = {10.1093/infdis/jis920},
  language = {eng},
}