Unknown,Transcriptomics,Genomics,Proteomics

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Role of interleukin-4 in the licensing of dendritic cells for the induction of Th2 responses [A]


ABSTRACT: T helper type 2 (Th2) responses are crucial for defense against infections by helminths and are responsible for the development of allergic reactions that can lead to severe clinical disorders, such as asthma or anaphylaxis, and ultimately to death. The induction of Th2 responses requires a specific activation process, triggered by specialized dendritic cells (DCs), by which naive CD4+ Th0 cells acquire the capacity to produce Th2 cytokines. However, the mechanistic basis of the functional specialization enabling DCs for the initiation of Th2 responses has remained elusive. Here we show that interleukin-4 (IL-4), a cytokine produced by basophils, mast cells and Th2-polarized CD4+ T helper cells, exerting a crucial function during anti-helminths and allergic Th2 responses, has a key role in the licensing/conditioning of DCs for the induction of Th2 responses, by bloking their potential to produce Th1-driving cytokines, such as IL-12, IL-18 and IL-23. Microarray analyses (duplicates) were for two types of comparisons: 1. moDCs stimulated with LPS from Escherichia coli versus C-moDCs non stimulated (control). 2. moDCs stimulated with LPS from Escherichia coli in presence of IL4 versus C-moDCs non stimulated (control).

ORGANISM(S): Mus musculus

SUBMITTER: Juan Oliveros 

PROVIDER: E-GEOD-39862 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

IL-4 blocks TH1-polarizing/inflammatory cytokine gene expression during monocyte-derived dendritic cell differentiation through histone hypoacetylation.

López-Bravo María M   Minguito de la Escalera María M   Domínguez Pilar M PM   González-Cintado Leticia L   del Fresno Carlos C   Martín Pilar P   Martínez del Hoyo Gloria G   Ardavín Carlos C  

The Journal of allergy and clinical immunology 20131017 6


<h4>Background</h4>Whereas recent research has characterized the mechanism by which dendritic cells (DCs) induce T(H)1/T(H)17 responses, the functional specialization enabling DCs to polarize T(H)2 responses remains undefined. Because IL-4 is essential during T(H)2 responses not only by acting on CD4(+) T cells through the activation of GATA-3 but also by regulating IgE class-switching, epithelial cell permeability, and muscle contractility, we hypothesized that IL-4 could also have a role in th  ...[more]

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