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Verfasst von:Ring, Sabine [VerfasserIn]   i
 Enk, Alexander [VerfasserIn]   i
 Mahnke, Karsten [VerfasserIn]   i
Titel:ATP activates regulatory T cells in vivo during contact hypersensitivity reactions
Verf.angabe:Sabine Ring, Alexander H. Enk, and Karsten Mahnke
E-Jahr:2010
Jahr:April 01 2010
Umfang:9 S.
Fussnoten:Gesehen am 24.05.2023
Titel Quelle:Enthalten in: The journal of immunology
Ort Quelle:Bethesda, Md. : Soc., 1916
Jahr Quelle:2010
Band/Heft Quelle:184(2010), 7, Seite 3408-3416
ISSN Quelle:1550-6606
Abstract:CD4+CD25+Foxp3+ regulatory T cells (Tregs) require activation to develop their full suppressive capacity. Similar to conventional T cells, Tregs can be activated via their TCRs; however, other means may be in place. We injected naive and nonactivated Tregs, being CD69−CD44lowCD62L+ into mice, and analyzed their phenotype after sensitization or challenge with the contact sensitizer 2,4,6-trinitro-1-chlorobenzene. We found that Tregs acquired an activated phenotype (CD69+CD44highCD62L−) in the draining lymph node after sensitization. In contrast, Ag challenge activated Tregs in the blood. This tissue-specific activation was induced by ATP, which was released at the respective tissue sites after sensitization or challenge, respectively. To demonstrate that activation was also essential for the induction of the suppressive function of Tregs, Tregs were treated with ATP receptor antagonists. In this study, we show that ATP receptor antagonists abrogated the suppressive effects of injected naive Tregs in contact hypersensitivity reactions. Thus, these data indicate that activation of Tregs via ATP in vivo provides a novel pathway of stimulating the suppressive function of Tregs.
DOI:doi:10.4049/jimmunol.0901751
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.4049/jimmunol.0901751
 DOI: https://doi.org/10.4049/jimmunol.0901751
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1846099749
Verknüpfungen:→ Zeitschrift

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