Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 42, Issue 5, Pages 1174-1179Publisher
WILEY
DOI: 10.1002/eji.201142216
Keywords
EAE; Foxp3; IL-6; IL-17; Treg cells
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Funding
- UK Medical Research Council
- German Research Foundation [SFB621, KFO250]
- MRC [G0901697, G0801924] Funding Source: UKRI
- Medical Research Council [G0901697, G0801924] Funding Source: researchfish
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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 a 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.
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