ID: 250. Issue 1 (November 2015)

• Record Type: Journal Article
• Authors: Tomisawa, Mio Angelica; Redpath, Stephen A.; Fonseca, Nicolette M.; Perona-Wright, Georgia
• Is Part Of: Cytokine. Volume 76:Issue 1(2015)
• Page Start: 111
• Publication Date: 2015-11
• Subjects: Cytokines -- Periodicals; 571.844
• DOI: 10.1016/j.cyto.2015.08.253
• Languages: English
• ISSNs: 1043-4666

Abstract

<abstract xml:lang="en" abstract-type="author" id="ab005"> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <p id="sp005">Surviving infection requires a careful balance of pro-inflammatory signals that promote pathogen clearance and anti-inflammatory signals that prevent immunopathology. The activation and expansion of regulatory T cells (Treg) is key to this balance. FoxP3+ Treg have been shown to acquire certain characteristics of effector T cells when activated in polarized immune responses, expressing Tbet during a Th1 infection and acquiring GATA3 expression during a Th2 response. It is controversial whether these new transcription factors are evidence of conversion to pro-inflammatory effector T cells, or are a mechanism by which the Treg become adapted to their environment and acquire enhanced suppressive function. We have observed that, during respiratory infection with Influenza A virus, approximately 30% of FoxP3+ Treg expressed the potent immunosuppressive cytokine, IL-10. All of the IL-10+ Tregs were also positive for Tbet. Our hypothesis is that the same cytokine signals needed for the induction of IL-10 are also responsible for the initiation of Tbet expression, suggesting that the adaption of Treg cells to their environment facilitates better immunosuppression. We will examine the effects of IL-12, IL-27 and other inflammatory signals on the Tbet expression, IL-10 production and suppressive function of FoxP3+ Tregs both in vitro and in vivo. Our data will elucidate the molecular signals required for optimal disease protection by FoxP3 Tregs in vivo.</p> </sec> </abstract>