PuSH - Publication Server of Helmholtz Zentrum München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Hoefig, K.P. ; Heissmeyer, V.

Posttranscriptional regulation of T helper cell fate decisions.

J. Cell Biol. 217, 2615-2631 (2018)
Publ. Version/Full Text DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
T helper cell subsets orchestrate context- and pathogen-specific responses of the immune system. They mostly do so by secreting specific cytokines that attract or induce activation and differentiation of other immune or nonimmune cells. The differentiation of T helper 1 (Th1), Th2, T follicular helper, Th17, and induced regulatory T cell subsets from naive T cells depends on the activation of intracellular signal transduction cascades. These cascades originate from T cell receptor and costimulatory receptor engagement and also receive critical input from cytokine receptors that sample the cytokine milieu within secondary lymphoid organs. Signal transduction then leads to the expression of subset-specifying transcription factors that, in concert with other transcription factors, up-regulate downstream signature genes. Although regulation of transcription is important, recent research has shown that posttranscriptional and posttranslational regulation can critically shape or even determine the outcome of Th cell differentiation. In this review, we describe how specific microRNAs, long noncoding RNAs, RNA-binding proteins, and ubiquitin-modifying enzymes regulate their targets to skew cell fate decisions.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
8.784
1.749
15
18
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Review
Keywords Ror-gamma-t; Experimental Autoimmune Encephalomyelitis; Messenger-rna Decay; Binding Protein Hur; Nf-kappa-b; Induced Cytidine Deaminase; Transcription Factor Foxp3; Aryl-hydrocarbon Receptor; Cytokine Gene-expression; Th17 Immune-response
Language english
Publication Year 2018
HGF-reported in Year 2018
ISSN (print) / ISBN 0021-9525
e-ISSN 1540-8140
Journal Journal of Cell Biology, The
Quellenangaben Volume: 217, Issue: 8, Pages: 2615-2631 Article Number: , Supplement: ,
Publisher Rockefeller University Press
Publishing Place 950 Third Ave, 2nd Flr, New York, Ny 10022 Usa
Reviewing status Peer reviewed
Institute(s) Research Unit Molecular Immune Regulation (AMIR)
POF-Topic(s) 30203 - Molecular Targets and Therapies
Research field(s) Immune Response and Infection
PSP Element(s) G-501712-001
DOI 10.1083/jcb.201708075
WOS ID WOS:000440809000006
PubMed ID 29685903
Erfassungsdatum 2018-06-25
[➜Report correction]