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- W4313351731 abstract "Abstract The aryl hydrocarbon receptor (AhR) is a promising target for the treatment of immune-mediated diseases. Activation of AhR by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in potent immunosuppression in a murine graft versus host (GVH) model, concurrent with a CD4+ regulatory phenotype characterized by increased expression of CTLA-4. CTLA-4 is associated with induction of indoleamine 2,3-dioxygenase (IDO) via IFNγ, resulting in decreased T-cell proliferation and immunosuppression. Treatment with TCDD has also been shown to induce IDO, suggesting that the TCDD-mediated up-regulation of CTLA-4 on donor cells may be responsible for the induction of IDO. Our results show that increased expression of CTLA-4 on donor CD4+ T-cells was concurrent with increased IFNγ, and significant up-regulation of the genes encoding IDO, Ido and Ido2. However, antibody blockade of CTLA-4 did not prevent the suppression of the CTL response by TCDD, suggesting that increased expression of CTLA-4 was not essential for the immunosuppressive effects. A direct role for increased IDO expression in TCDD-mediated immunosuppression is currently under investigation." @default.
- W4313351731 created "2023-01-06" @default.
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- W4313351731 date "2012-05-01" @default.
- W4313351731 modified "2023-10-18" @default.
- W4313351731 title "Effect of AhR activation by TCDD on the immunosuppressive CTLA-4 - IFNγ - IDO pathway (176.5)" @default.
- W4313351731 doi "https://doi.org/10.4049/jimmunol.188.supp.176.5" @default.
- W4313351731 hasPublicationYear "2012" @default.
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