| Interleukin-10 promotes NK cell killing of autologous macrophages by stimulating expression of NKG2D ligands. | |
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MedLine Citation:
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PMID: 20883317 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Under inflammatory conditions, the pleiotropic cytokine interleukin-10 (IL-10) is released in many tissues. It mediates anti-inflammatory effects in particular by inhibiting the release of T helper type 1 (Th1) cytokines. In contrast, we show here that NK cell cytotoxicity against autologous macrophages is elevated if both cell types are cultured with IL-10. The expression of most activatory NK receptors is increased after culture in the presence of IL-10. On the other hand, macrophages cultured in the presence of IL-10 show elevated expression of the NKG2D ligands major histocompatibility complex (MHC) class 1-like molecules (MIC) - A and - B, as well as UL-16 binding proteins (ULBP) - ULBP-1, ULBP-2 and ULBP-3. By masking the interaction of NK cells with macrophages through interruption of the NKG2D receptor with its ligands, we could reverse the IL-10-induced lysis of macrophages. Our data therefore reveal that IL-10 may exert a novel immunomodulatory role by stimulating NKG2D ligand expression on macrophages, thereby rendering them susceptible to NK cell elimination. This suggests that NK cells would delete macrophages and potentially other immature antigen-presenting cells (APC) or their precursors under inflammatory conditions as a feedback mechanism to shut off uncontrolled immune responses. |
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Authors:
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U Schulz; M Kreutz; G Multhoff; B Stoelcker; M Köhler; R Andreesen; E Holler |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Scandinavian journal of immunology Volume: 72 ISSN: 1365-3083 ISO Abbreviation: Scand. J. Immunol. Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-10-04 Completed Date: 2010-11-04 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0323767 Medline TA: Scand J Immunol Country: England |
Other Details:
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Languages: eng Pagination: 319-31 Citation Subset: IM |
Copyright Information:
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© 2010 The Authors. Scandinavian Journal of Immunology © 2010 Blackwell Publishing Ltd. |
Affiliation:
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Department of Hematology and Oncology, University of Regensburg, Regensburg, Germany. Ute.Schulz@klinik.uni-regensburg.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antibodies, Monoclonal
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pharmacology Cells, Cultured Cytotoxicity, Immunologic / drug effects*, immunology Flow Cytometry Humans Intercellular Signaling Peptides and Proteins / genetics, immunology, metabolism* Interleukin-10 / pharmacology* K562 Cells Killer Cells, Natural / drug effects*, immunology, metabolism Macrophages / drug effects*, immunology, metabolism Monocytes / drug effects, immunology, metabolism NK Cell Lectin-Like Receptor Subfamily K / genetics, metabolism RNA, Messenger / genetics, metabolism Reverse Transcriptase Polymerase Chain Reaction |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Monoclonal; 0/Intercellular Signaling Peptides and Proteins; 0/KLRK1 protein, human; 0/NK Cell Lectin-Like Receptor Subfamily K; 0/RNA, Messenger; 0/ULBP2 protein, human; 130068-27-8/Interleukin-10 |
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