02222nas a2200457 4500000000100000008004100001260001600042653002500058653001800083653002500101653001500126653002000141653001100161653002300172653002100195653001900216653003100235653002500266653002500291653001600316653001400332653002500346653001900371100001200390700001500402700001300417700001200430700001500442700001000457700001000467700001200477700001000489700001400499700001400513700001100527245007200538300001100610490000800621520112100629022001401750 2013 d c2013 Mar 1510aAntigen Presentation10aAntigens, CD110aCell Differentiation10aGalectin 310aGene Expression10aHumans10aImmunity, Cellular10aImmunity, Innate10aInterleukin-1010aInterleukin-12 Subunit p4010aLeprosy, lepromatous10aLeprosy, Tuberculoid10aMacrophages10aMonocytes10aMycobacterium leprae10aRNA, Messenger1 aChung A1 aSieling PA1 aSchenk M1 aTeles R1 aKrutzik SR1 aHsu D1 aLiu F1 aSarno E1 aRea T1 aStenger S1 aModlin RL1 aLee DJ00aGalectin-3 regulates the innate immune response of human monocytes. a947-560 v2073 a
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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