Cutting Edge: Mincle Is Essential for Recognition and Adjuvanticity of the Mycobacterial Cord Factor and its Synthetic Analog Trehalose-Dibehenate
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- Hanne Schoenen
- Institute of Clinical Microbiology, Immunology and Hygiene
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- Barbara Bodendorfer
- Institute of Clinical Microbiology, Immunology and Hygiene
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- Kelly Hitchens
- Griffith University , Queensland,
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- Silvia Manzanero
- Griffith University , Queensland,
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- Kerstin Werninghaus
- Institute of Clinical Microbiology, Immunology and Hygiene
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- Falk Nimmerjahn
- Division of Rheumatology and Immunology, Medical Department, Friedrich-Alexander-Universität Erlangen-Nürnberg and University Clinics of Erlangen , Erlangen
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- Else Marie Agger
- Adjuvant Research, Department of Infectious Disease Immunology, Statens Serum Institut , Copenhagen,
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- Steffen Stenger
- Institute of Medical Microbiology, University Hospital Ulm , Ulm
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- Peter Andersen
- Adjuvant Research, Department of Infectious Disease Immunology, Statens Serum Institut , Copenhagen,
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- Jürgen Ruland
- Department of Hematology, Technical University Munich , Munich,
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- Gordon D Brown
- Section of Immunology and Infection, Division of Applied Medicine, Institute of Medical Sciences, University of Aberdeen , Aberdeen,
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- Christine Wells
- Griffith University , Queensland,
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- Roland Lang
- Institute of Clinical Microbiology, Immunology and Hygiene
書誌事項
- 公開日
- 2010-03
- 権利情報
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- https://academic.oup.com/pages/standard-publication-reuse-rights
- DOI
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- 10.4049/jimmunol.0904013
- 公開者
- Oxford University Press (OUP)
この論文をさがす
説明
<jats:title>Abstract</jats:title> <jats:p>The mycobacterial cord factor trehalose-6,6-dimycolate (TDM) and its synthetic analog trehalose-6,6-dibehenate (TDB) are potent adjuvants for Th1/Th17 vaccination that activate Syk-Card9 signaling in APCs. In this study, we have further investigated the molecular mechanism of innate immune activation by TDM and TDB. The Syk-coupling adapter protein FcRγ was essential for macrophage activation and Th17 adjuvanticity. The FcRγ-associated C-type lectin receptor Mincle was expressed in macrophages and upregulated by TDM and TDB. Recombinant Mincle-Fc fusion protein specifically bound to the glycolipids. Genetic ablation of Mincle abolished TDM/TDB-induced macrophage activation and induction of T cell immune responses to a tuberculosis subunit vaccine. Macrophages lacking Mincle or FcRγ were impaired in the inflammatory response to Mycobacterium bovis bacillus Calmette-Guérin. These results establish that Mincle is a key receptor for the mycobacterial cord factor and controls the Th1/Th17 adjuvanticity of TDM and TDB.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 184 (6), 2756-2760, 2010-03
Oxford University Press (OUP)
