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The microRNA cluster miR-17∼92 promotes TFH cell differentiation and represses subset-inappropriate gene expression

Baumjohann, Dirk and Kageyama, Robin and Clingan, Jonathan M. and Morar, Malika M. and Patel, Sana and de Kouchkovsky, Dimitri and Bannard, Oliver and Bluestone, Jeffrey A. and Matloubian, Mehrdad and Ansel, K. Mark and Jeker, Lukas T.. (2013) The microRNA cluster miR-17∼92 promotes TFH cell differentiation and represses subset-inappropriate gene expression. Nature Immunology, 14 (8). pp. 840-848.

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Official URL: https://edoc.unibas.ch/61959/

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Abstract

Follicular helper T cells (TFH cells) are the prototypic helper T cell subset specialized to enable B cells to form germinal centers (GCs) and produce high-affinity antibodies. We found that expression of microRNAs (miRNAs) by T cells was essential for TFH cell differentiation. More specifically, we show that after immunization of mice with protein, the miRNA cluster miR-17∼92 was critical for robust differentiation and function of TFH cells in a cell-intrinsic manner that occurred regardless of changes in proliferation. In a viral infection model, miR-17∼92 restrained the expression of genes 'inappropriate' to the TFH cell subset, including the direct miR-17∼92 target Rora. Removal of one Rora allele partially 'rescued' the inappropriate gene signature in miR-17∼92-deficient TFH cells. Our results identify the miR-17∼92 cluster as a critical regulator of T cell-dependent antibody responses, TFH cell differentiation and the fidelity of the TFH cell gene-expression program.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Molecular Immune Regulation (Jeker)
UniBasel Contributors:Jeker, Lukas T.
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Nature Publishing Group
ISSN:1529-2916
e-ISSN:1529-2916
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:16 Dec 2020 07:51
Deposited On:16 Dec 2020 07:51

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