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Posttranscriptional regulation of T helper cell fate decisions.

J. Cell Biol. 217, 2615-2631 (2018)
Verlagsversion DOI
Open Access Gold (Paid Option)
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter 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
ISSN (print) / ISBN 0021-9525
e-ISSN 1540-8140
Quellenangaben Band: 217, Heft: 8, Seiten: 2615-2631 Artikelnummer: , Supplement: ,
Verlag Rockefeller University Press
Verlagsort 950 Third Ave, 2nd Flr, New York, Ny 10022 Usa
Begutachtungsstatus Peer reviewed