About: Human TSLP and TLR3 ligands promote differentiation of Th17 cells with a central memory phenotype under Th2‐polarizing conditions

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About: Human TSLP and TLR3 ligands promote differentiation of Th17 cells with a central memory phenotype under Th2‐polarizing conditions Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Human TSLP and TLR3 ligands promote differentiation of Th17 cells with a central memory phenotype under Th2‐polarizing conditions
Creator	Chiba, T Nishio, A Tanaka Ãw, J Watanabe Ãw, N
Source	Medline; PMC
abstract	Background Human thymic stromal lymphopoietin (TSLP) is expressed in the human asthmatic lung and activates dendritic cells (DCs) to strongly induce proallergic T‐helper type 2 (Th2) cell responses, suggesting that TSLP plays a critical role in the pathophysiology of human asthma. Th2 cells are predominantly involved in mild asthma, whereas a mixture of Th1 and Th2 cells with neutrophilic inflammation, probably induced by Th17, affects more severe asthmatic disease. Exacerbation of asthmatic inflammation is often triggered by airway‐targeting RNA viral infection; virus‐derived double‐stranded RNA, Toll‐like receptor (TLR)3 ligand, activates bronchial epithelial cells to produce pro‐inflammatory mediators, including TSLP. Objective Because TSLPR‐expressing DCs express TLR3, we examined how the relationship between TSLP and TLR3 ligand stimulation influences DC activation. Methods CD11c(+)DCs purified from adult peripheral blood were cultured in TLR ligands containing media with or without TSLP and then co‐cultured with allogeneic naïve CD4(+)T cells. Results CD11c(+) DCs responded to a combination of TSLP and TLR3 ligand, poly(I : C), to up‐regulate expression of the functional TSLP receptor and TLR3. Although TSLP alone did not induce IL‐23 production by DCs, poly(I : C) alone primed DCs for the production of IL‐23, and a combination of TSLP and poly(I : C) primed DCs for further production of IL‐23. The addition of poly(I : C) did not inhibit TSLP‐activated DCs to prime naïve CD4(+) T cells to differentiate into inflammatory Th2 cells. Furthermore, DCs activated by a combination of TSLP and poly(I : C) primed more naïve CD4(+) T cells to differentiate into Th17‐cytokine–producing cells with a central memory T cell phenotype compared with DCs activated by poly(I : C) alone. Conclusions These results suggest that through DC activation, human TSLP and TLR3 ligands promote differentiation of Th17 cells with the central memory T cell phenotype under Th2‐polarizing conditions.
has issue date	2008-12-01(xsd:dateTime)
bibo:doi	10.1111/j.1365-2222.2008.03151.x
bibo:pmid	19055649
has license	no-cc
sha1sum (hex)	c7a3db768fbae9595890043e86bdec9de4d1227c
schema:url	https://doi.org/10.1111/j.1365-2222.2008.03151.x
resource representing a document's title	Human TSLP and TLR3 ligands promote differentiation of Th17 cells with a central memory phenotype under Th2‐polarizing conditions
has PubMed Central identifier	PMC7164823
has PubMed identifier	19055649
schema:publication	Clin Exp Allergy
resource representing a document's body	covid:c7a3db768fbae9595890043e86bdec9de4d1227c#body_text
is schema:about of	named entity 'DCs' named entity 'Th2 cells' named entity 'ligands' named entity 'phenotype' named entity 'stimulation' named entity 'activated' named entity 'Th17' named entity 'TLR3' named entity 'asthmatic' named entity 'CD4' named entity 'differentiation' named entity 'Human' named entity 'Th2' named entity 'AIRWAY' named entity 'CD11C' named entity 'TSLPR' named entity 'CENTRAL MEMORY T CELL' named entity 'ASTHMA' named entity 'VIRUS' named entity 'ADDITION' named entity 'RELATIONSHIP' named entity '293' named entity 'HOW' named entity 'OBJECTIVE' named entity 'DERIVED' named entity 'INDUCE' named entity 'TSLP RECEPTOR' named entity 'BACKGROUND' named entity 'PRODUCTION' named entity 'IL-23 PRODUCTION' named entity 'DENDRITIC CELLS' named entity 'RESPONSES' named entity 'PRO-INFLAMMATORY MEDIATORS' named entity 'STIMULATION' named entity 'TSLP' named entity 'TO PRODUCE' named entity 'EXACERBATION' named entity 'TLR3' named entity 'PLAYS' named entity 'COMBINATION' covid:arg/c7a3db768fbae9595890043e86bdec9de4d1227c named entity 'inflammation' named entity 'Th17' named entity 'Th1' named entity 'inhibit' named entity 'neutrophilic' named entity 'bronchial epithelial cells' named entity 'T cells' named entity 'express' named entity 'inflammation' named entity 'DCs' named entity 'induce' named entity 'poly' named entity 'responded' named entity 'polarizing' named entity 'ligand' named entity 'IL-23' named entity 'DCs' named entity 'TSLP' named entity 'TSLPR' named entity 'asthmatic' named entity 'TSLP' named entity 'Th17' named entity 'CD4' named entity 'TLR3' named entity 'viral infection' named entity 'memory T cell' named entity 'Th1' named entity 'memory T cell' named entity 'inflammation' named entity 'phenotype' named entity 'inflammatory mediators' named entity 'type 2' named entity 'IL-23' named entity 'DCs' named entity 'cytokine' named entity 'human asthma' named entity 'TSLP'

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