Control of Treg and TH17 cell differentiation by the aryl hydrocarbon receptor

@article{Quintana2008ControlOT,
  title={Control of Treg and TH17 cell differentiation by the aryl hydrocarbon receptor},
  author={Francisco J. Quintana and Alexandre Salgado Basso and Antonio H. Iglesias and Thomas Korn and Mauricio Franco Farez and Estelle Bettelli and Mario C{\'a}ccamo and Mohamed Oukka and Howard L. Weiner},
  journal={Nature},
  year={2008},
  volume={453},
  pages={65-71}
}
Regulatory T cells (Treg) expressing the transcription factor Foxp3 control the autoreactive components of the immune system. The development of Treg cells is reciprocally related to that of pro-inflammatory T cells producing interleukin-17 (TH17). Although Treg cell dysfunction and/or TH17 cell dysregulation are thought to contribute to the development of autoimmune disorders, little is known about the physiological pathways that control the generation of these cell lineages. Here we report… 
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Activation of the aryl hydrocarbon receptor induces human type 1 regulatory T cell–like and Foxp3+ regulatory T cells
TLDR
It is found that AhR activation promoted the differentiation of CD4+Foxp3− T cells, which produce IL-10 and control responder T cells through granzyme B, and is a potential target through which functional iTreg cells could be induced in human autoimmune disorders.
Cytokine Regulation in Human CD4 T Cells by the Aryl Hydrocarbon Receptor and Gq-Coupled Receptors
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The AhR-dependent transcriptome in human CD4 T cells is studied and it is suggested the mechanism through which the AhR regulates T cell function may be partially dependent on Gq-coupled receptors including GPR68.
Type 1 regulatory T cells (Tr1) in autoimmunity.
TLDR
How ligands that bind to AhR and affect the biology of IL-27-induced Tr1 cells can be exploited as a therapeutic approach to alleviate human autoimmune diseases is discussed.
T cells: Tuning T cells through the aryl hydrocarbon receptor
  • S. Allan
  • Chemistry
    Nature Reviews Immunology
  • 2008
immune tolerance and inflammation, regulatory T (TReg) cells and interleukin‐17 (IL‐17)‐producing CD4+ T helper cells (TH17 cells) are areas of intensive study. Two new reports in Nature have now…
Role of Aryl Hydrocarbon Receptor (AhR) in the Regulation of Immunity and Immunopathology During Trypanosoma cruzi Infection
TLDR
A model in which a threshold of AhR activation exists is proposed and may explain how activation or inhibition of Ahr-derived signals by infection/inflammation-induced ligands, therapeutic interventions or exposure to pollutants can modulate infections/diseases outcomes or vaccination efficacy.
The roles of aryl hydrocarbon receptor in immune responses.
TLDR
The roles of Ahr in macrophages and T cells are discussed and studies examining Ahr activation in other cell types have revealed additional contributions to B cell and osteoblast/osteoclast differentiation.
Generation of IL-8 and IL-9 Producing CD4+ T Cells Is Affected by Th17 Polarizing Conditions and AHR Ligands
TLDR
It is found that a high proportion of T helper cells cultured under Th17 polarizing conditions are IL-8 and IL-9 single producing cells and that AHR activation results in an upregulation of IL- 8 and a downregulation ofIL-9 production.
The Aryl hydrocarbon Receptor (AhR) interacts with c-Maf to promote the differentiation of IL-27-induced regulatory type 1 (TR1) cells
TLDR
It is shown that the ligand-activated transcription factor aryl hydrocarbon receptor (AhR), which was induced by IL-27, acted in synergy with c-Maf to promote the development of Tr1 cells and the amelioration of experimental autoimmune encephalomyelitis.
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.
Suppression of experimental autoimmune uveoretinitis by inducing differentiation of regulatory T cells via activation of aryl hydrocarbon receptor.
TLDR
Activation of AHR by TCDD markedly suppressed autoimmune uveoretinitis through mechanisms that expand CD25(+)Foxp3(+) T(reg) cells and interfere with the activation of Th1 and Th17 cells.
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