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Regulated expression of nuclear receptor ROR t confers distinct functional fates to NK cell receptor-expressing ROR t(+) innate lymphocytes

Vonarbourg, Cedric and Mortha, Arthur and Bui, Viet L. and Hernandez, Pedro P. and Kiss, Elina A. and Hoyler, Thomas and Flach, Melanie and Bengsch, Bertram and Thimme, Robert and Hölscher, Christoph and Hönig, Manfred and Pannicke, Ulrich and Schwarz, Klaus and Ware, Carl F. and Finke, Daniela and Diefenbach, Andreas. (2010) Regulated expression of nuclear receptor ROR t confers distinct functional fates to NK cell receptor-expressing ROR t(+) innate lymphocytes. Immunity, Vol. 33, H. 5. pp. 736-751.

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Official URL: http://edoc.unibas.ch/dok/A6004247

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Abstract

Whether the recently identified innate lymphocyte population coexpressing natural killer cell receptors (NKRs) and the nuclear receptor ROR t is part of the NK or lymphoid tissue inducer (LTi) cell lineage remains unclear. By using adoptive transfer of genetically tagged LTi-like cells, we demonstrate that NKR ? ROR t(+) innate lymphocytes but not NK cells were direct progenitors to NKR(+)ROR t(+) cells in vivo. Genetic lineage tracing revealed that the differentiation of LTi-like cells was characterized by the stable upregulation of NKRs and a progressive loss of ROR t expression. Whereas interleukin-7 (IL-7) and intestinal microbiota stabilized ROR t expression within such NKR-LTi cells, IL-12 and IL-15 accelerated ROR t loss. ROR t(+) NKR-LTi cells produced IL-22, whereas ROR t ? NKR-LTi cells released IFN- and were potent inducers of colitis. Thus, the ROR t gradient in NKR-LTi cells serves as a tunable rheostat for their functional program. Our data also define a previously unappreciated role of ROR t ? NKR-LTi cells for the onset or maintenance of inflammatory bowel diseases.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Children's Hospital > Developmental Immunology (Finke)
UniBasel Contributors:Finke, Daniela
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Cell Press
ISSN:1074-7613
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:07 Dec 2012 13:04
Deposited On:07 Dec 2012 13:03

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