Reciprocal TH17 and Regulatory T Cell Differentiation Mediated by Retinoic Acid

@article{Mucida2007ReciprocalTA,
  title={Reciprocal TH17 and Regulatory T Cell Differentiation Mediated by Retinoic Acid},
  author={Daniel Mucida and Yunji Park and Gisen Kim and O. V. Turovskaya and Iain Scott and Mitchell Kronenberg and Hilde Cheroutre},
  journal={Science},
  year={2007},
  volume={317},
  pages={256 - 260}
}
The cytokine transforming growth factor–β (TGF-β) converts naïve T cells into regulatory T (Treg) cells that prevent autoimmunity. However, in the presence of interleukin-6 (IL-6), TGF-β has also been found to promote the differentiation of naïve T lymphocytes into proinflammatory IL-17 cytokine-producing T helper 17 (TH17) cells, which promote autoimmunity and inflammation. This raises the question of how TGF-β can generate such distinct outcomes. We identified the vitamin A metabolite… Expand
TGFβ and Retinoic Acid Intersect in Immune-Regulation
TLDR
A vitamin A metabolite, retinoic acid, was recently identified as a key modulator of TGFβ-driven immune deviation capable of suppressing TH17 differentiation while promoting Foxp3+Treg generation 6-10 and suggests that a sensitive regulatory mechanism must exist to control TGF β-driven TH17 effector and Treg differentiation. Expand
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RA is described as a key modulator of TGF-β-driven immune deviation capable of suppressing TH17 differentiation while promoting Foxp3+ Treg generation and how RA can affect mucosal immune regulation is discussed. Expand
Transcriptional regulation of Th17 cell differentiation.
TLDR
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Regulatory T cells: Reciprocal regulation by retinoic acid
  • O. Leavy
  • Biology
  • Nature Reviews Immunology
  • 2007
TLDR
It is shown that the vitamin A metabolite retinoic acid is a key regulator of TGFβ-induced T-cell differentiation and has important implications for the understanding of vitamin A deficiency and highlights the therapeutic potential of retinosic acid in diseases in which there is an imbalance in the numbers of T GFβ-dependent TH17 cells and regulatory T cells. Expand
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TLDR
TGFβ1 acts as a pro-inflammatory cytokine and induces interleukin (IL)-17-producing pathogenic T-helper cells (Th IL-17 cells) synergistically during an inflammatory response in which IL-6 is produced. Expand
TGF-β function in immune suppression.
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Recent studies suggest that Smad2 as well as Smad3 play essential roles in Foxp3 induction and cytokine suppression, whereas Th17 differentiation is promoted via the Smad-independent pathway. Expand
Contextual regulation of inflammation: a duet by transforming growth factor-beta and interleukin-10.
TLDR
The collective activity of TGF-beta and IL-10 ensures a controlled inflammatory response specifically targeting pathogens without evoking excessive immunopathology to self-tissues. Expand
Th17 cells in inflammation.
TLDR
The IL-17-producing T helper (Th17) cell has been recently identified as a new subset of the T helper cell and a mediator of inflammation associated with various autoimmune diseases. Expand
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