2016
DOI: 10.1038/ncomms10888
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IL-15-dependent balance between Foxp3 and RORγt expression impacts inflammatory bowel disease

Abstract: The ability of CD4+ T cells to change their phenotype and to specialize into different functional subsets may enhance the risk of autoimmune diseases. Here we investigate how a pleiotropic cytokine interleukin (IL)-15 may modify the functional commitment of CD4+ T cells expressing the lineage-associated transcription factors: forkhead box P3 (Foxp3; Treg) and RORγt (Th17) in the context of inflammatory bowel disease (IBD). We demonstrate in mice that impaired delivery of IL-15 to CD4+ T cells in the colon down… Show more

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Cited by 68 publications
(66 citation statements)
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References 42 publications
(60 reference statements)
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“…1D). Thus, contrary to previous reports [12, 26], our results indicate that IL-15 expression is not a feature associated with CD4 T cells, and therefore argue against an autocrine role for IL-15 in CD4 T cells.…”
Section: Resultscontrasting
confidence: 99%
See 2 more Smart Citations
“…1D). Thus, contrary to previous reports [12, 26], our results indicate that IL-15 expression is not a feature associated with CD4 T cells, and therefore argue against an autocrine role for IL-15 in CD4 T cells.…”
Section: Resultscontrasting
confidence: 99%
“…Surprisingly, and in contrast to previous studies [12, 26], Il15 gene reporter mice analysis and quantitative real-time RT-PCR results failed to provide evidence for IL-15 expression in CD4 T cells. Moreover, CD4 T cells did not express IL-15Rα, which is the high-affinity receptor required for IL-15 trans -presentation to IL-2Rβ/γc expressing target cells [27, 28], and which is required for optimal IL-15 signaling in cis [20, 29, 30].…”
Section: Introductioncontrasting
confidence: 99%
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“…The last factor for the pathogenesis and progression of IBD that deserves to be mentioned here is the adaptive immune response. It is generally acknowledged that increased pro-inflammatory cytokines produced by the T-helper cells or decreased anti-inflammatory cytokines induced by ineffective regulatory T-cells contribute to the pathogenesis of IBD (23, 24). Nevertheless, since the pathogenesis of IBD is complex and the exact underlying mechanisms still remain unclear, no effective therapeutic strategies have been developed for the treatment of IBD.…”
Section: Pathogenesis Of Ibdmentioning
confidence: 99%
“…Tregs can be divided into nature Tregs (nTregs) and induced Tregs (iTregs), both of which have been shown to play key roles in a variety of immune diseases including hepatic ischemia-reperfusion injury (IRI), acute hepatic damage, acute graft-versus-host disease, inflammatory bowel disease (IBD), systemic lupus erythematosus (SLE), rheumatoid arthritis, and chronic obstructive pulmonary disease (Tosiek et al, 2016;Miyara et al, 2014;Okamura et al, 2015;Salter, 1989). However, the stability of Tregs has long been controversial; some evidence demonstrates that Tregs may be unstable and dysfunctional, especially in an inflammatory environment, in which Tregs can readily transform into T-helper (Th) cells such as Th1, Th2, Th17, and Tfh cells and accelerate inflammatory reactions, thereby exacerbating the underlying disease (Feuerer et al, 2009;Wan and Flavell, 2007;Lu et al, 2010).…”
Section: Introductionmentioning
confidence: 99%