Stable form of galectin-9, a Tim-3 ligand, inhibits contact hypersensitivity and psoriatic reactions : a potent therapeutic tool for Th1- and/or Th17-mediated skin inflammation
Tim-3 is a cell surface molecule preferentially expressed in Th1 and Th17 cells. Galectin-9 is a ligand for Tim-3 and the binding of galectin-9 to Tim-3 induces apoptosis. We recently developed a stable form of galectin-9 (sGal-9) by partial deletion of the linker peptide. In this study, we characte...
Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 132(2009), 2 vom: 03. Aug., Seite 184-94 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2009
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Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
Schlagworte: | Journal Article Chemokines Cytokines Galectins Havcr2 protein, mouse Hepatitis A Virus Cellular Receptor 2 Interleukin-17 Interleukin-23 Ligands Receptors, Virus mehr... |
Zusammenfassung: | Tim-3 is a cell surface molecule preferentially expressed in Th1 and Th17 cells. Galectin-9 is a ligand for Tim-3 and the binding of galectin-9 to Tim-3 induces apoptosis. We recently developed a stable form of galectin-9 (sGal-9) by partial deletion of the linker peptide. In this study, we characterized the therapeutic effects of sGal-9 on inflammatory reactions in contact hypersensitivity and IL-23-induced psoriatic mouse models. In contact hypersensitivity in mice, the ear swelling response was suppressed by sGal-9. In vitro treatment with sGal-9 resulted in cell apoptosis of CD4, CD8, and hepatic NK cells. sGal-9-treated mice had decreased IFN-gamma- and IL-17-producing T cells. Similarly, sGal-9 reduced epidermal thickness and dermal cellular infiltrate levels in IL-23-induced psoriasis-like skin inflammation. This was accompanied by decreased skin lesion levels of IL-17 and IL-22. sGal-9 may be a unique and useful therapeutic tool for the treatment of Th1- and/or Th17-mediated skin inflammation |
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Beschreibung: | Date Completed 17.09.2009 Date Revised 25.11.2016 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1521-7035 |
DOI: | 10.1016/j.clim.2009.04.012 |