O'Connor, Richard A., Floess, Stefan, Huehn, Jochen, Jones, Simon Arnett ![]() |
Abstract
Foxp3+ T regulatory (Treg) cells can be induced to produce interleukin (IL)-17 by in vitro exposure to proinflammatory cytokines, drawing into question their functional stability at sites of inflammation. Unlike their splenic counterparts, Treg cells from the inflamed central nervous system (CNS-Treg cells) during EAE resisted conversion to IL-17 production when exposed to IL-6. We show that the highly activated phenotype of CNS-Treg cells includes elevated expression of the Th1-associated molecules CXCR3 and T-bet, but reduced expression of the IL-6 receptor α chain (CD126) and the signaling chain gp130. We found a lack of IL-6 receptor on all CNS CD4+ T cells, which was reflected by an absence of both classical and trans-IL-6 signaling in CNS CD4+ cells, compared with their splenic counterparts. We propose that extinguished responsiveness to IL-6 (via down-regulation of CD126 and gp130) stabilizes the regulatory phenotype of activated Treg cells at sites of autoimmune inflammation.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine Systems Immunity Research Institute (SIURI) |
Subjects: | Q Science > QR Microbiology > QR180 Immunology R Medicine > R Medicine (General) |
Uncontrolled Keywords: | EAE; Foxp3; IL-6; IL-17; Treg cells |
Publisher: | John Wiley & Sons |
ISSN: | 0014-2980 |
Last Modified: | 21 Oct 2022 10:49 |
URI: | https://orca.cardiff.ac.uk/id/eprint/41456 |
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