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231223s2009 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2009.04.012
|2 doi
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|a pubmed24n0629.xml
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|a (DE-627)NLM188739289
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|a (NLM)19464955
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Niwa, Haruna
|e verfasserin
|4 aut
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|a Stable form of galectin-9, a Tim-3 ligand, inhibits contact hypersensitivity and psoriatic reactions
|b a potent therapeutic tool for Th1- and/or Th17-mediated skin inflammation
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|c 2009
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 17.09.2009
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|a Date Revised 25.11.2016
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a 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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|a Journal Article
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|a Chemokines
|2 NLM
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|a Cytokines
|2 NLM
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|a Galectins
|2 NLM
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|a Havcr2 protein, mouse
|2 NLM
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|a Hepatitis A Virus Cellular Receptor 2
|2 NLM
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|a Interleukin-17
|2 NLM
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|a Interleukin-23
|2 NLM
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|a Ligands
|2 NLM
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|a Receptors, Virus
|2 NLM
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|a galectin 9, mouse
|2 NLM
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|a Croton Oil
|2 NLM
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|a 8001-28-3
|2 NLM
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|a Dinitrofluorobenzene
|2 NLM
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|a D241E059U6
|2 NLM
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|a Satoh, Takahiro
|e verfasserin
|4 aut
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1 |
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|a Matsushima, Yuki
|e verfasserin
|4 aut
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1 |
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|a Hosoya, Kazuki
|e verfasserin
|4 aut
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1 |
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|a Saeki, Kazumi
|e verfasserin
|4 aut
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1 |
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|a Niki, Toshiro
|e verfasserin
|4 aut
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1 |
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|a Hirashima, Mitsuomi
|e verfasserin
|4 aut
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|a Yokozeki, Hiroo
|e verfasserin
|4 aut
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773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 132(2009), 2 vom: 03. Aug., Seite 184-94
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
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|g volume:132
|g year:2009
|g number:2
|g day:03
|g month:08
|g pages:184-94
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|u http://dx.doi.org/10.1016/j.clim.2009.04.012
|3 Volltext
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 132
|j 2009
|e 2
|b 03
|c 08
|h 184-94
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