Interaction of Monocytes with NK Cells upon Toll-Like Receptor-Induced Expression of the NKG2D Ligand MICA
| Autor: | Alexander Steinle, Patrice Decker, Gundram Jung, Matthias Krusch, Katrin M. Baltz, Mercedes Kloss, Hans-Georg Rammensee, Tina Baessler, Helmut R. Salih |
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| Rok vydání: | 2008 |
| Předmět: |
Cytotoxicity
Immunologic Immunology Enzyme-Linked Immunosorbent Assay chemical and pharmacologic phenomena Ligands Monocytes Interferon-gamma Interleukin 21 medicine Humans Immunology and Allergy CXCL14 MHC class II biology Reverse Transcriptase Polymerase Chain Reaction Chemistry Monocyte Janus kinase 3 Histocompatibility Antigens Class I Toll-Like Receptors Histocompatibility Antigens Class II Receptor Cross-Talk Flow Cytometry NKG2D Molecular biology Cell biology Killer Cells Natural medicine.anatomical_structure NK Cell Lectin-Like Receptor Subfamily K B7-1 Antigen biology.protein Interleukin 12 Cytokines CD80 |
| Zdroj: | The Journal of Immunology. 181:6711-6719 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.181.10.6711 |
| Popis: | Reciprocal interactions between NK cells and dendritic cells have been shown to influence activation of NK cells, maturation, or lysis of dendritic cells and subsequent adaptive immune responses. However, little is known about the crosstalk between monocytes and NK cells and the receptors involved in this interaction. We report in this study that human monocytes, upon TLR triggering, up-regulate MHC class I-Related Chain (MIC) A, but not other ligands for the activating immunoreceptor NKG2D like MICB or UL-16 binding proteins 1–3. MICA expression was associated with CD80, MHC class I and MHC class II up-regulation, secretion of proinflammatory cytokines, and apoptosis inhibition, but was not accompanied by release of MIC molecules in soluble form. TLR-induced MICA on the monocyte cell surface was detected by autologous NK cells as revealed by NKG2D down-regulation. Although MICA expression did not render monocytes susceptible for NK cell cytotoxicity, LPS-treated monocytes stimulated IFN-γ production of activated NK cells which was substantially dependent on MICA-NKG2D interaction. No enhanced NK cell proliferation or cytotoxicity against third-party target cells was observed after stimulation of NK cells with LPS-activated monocytes. Our data indicate that MICA-NKG2D interaction constitutes a mechanism by which monocytes and NK cells as an early source of IFN-γ may communicate directly during an innate immune response to infections in humans. |
| Databáze: | OpenAIRE |
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