IDO1 Target Analysis Report Summary
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About the Target
IDO1 is an important enzyme involved in tryptophan catabolism through the kynurenine pathway. It can be upregulated by various factors such as IFN-gamma, TNF-alpha, and LPS, while downregulated by IL-4 and TGF-beta. Inhibitors of IDO1 have been extensively studied [1]. IDO1 inhibitors can increase T-cell activation at the site of tumor cells, making them potential therapeutic agents for cancer treatment [2]. Additionally, IDO1 activity plays a crucial role in the metabolism of tryptophan in the gastrointestinal tract, affecting mucosal defense, mucin production, and tight junction proteins [3]. Furthermore, IDO1 is involved in the anti-T. gondii immune response and its growth inhibition in human cells [4]. Combined neutralization of PD-L1 and TGF-beta1 with inhibition of IDO1 has been shown to reverse immune suppression in peritumoral cells [5].
In the context of the study, the researchers investigated the effects of kynurenic acid (KYNA), an IDO1 metabolite, on TSG-6 production in human umbilical cord mesenchymal stem cells (HUC-MSCs) through the activation of the aryl hydrocarbon receptor (AhR) signaling pathway [6]. They found that MSCs expressed high levels of AhR compared to other receptors [6a]. KYNA treatment led to increased translocation of AhR to the nucleus, suggesting the activation of AhR signaling in MSCs [6b]. This was further supported by the increased expression of AhR-regulated metabolic enzymes, CYP1A1 and CYP1B1 [6c]. KYNA also enhanced the binding of AhR to the TSG-6 promoter, promoting TSG-6 expression [6e]. The researchers observed that KYNA treatment resulted in enhanced TSG-6 production by HUC-MSCs [6d]. Additionally, KYNA inhibited immune cell infiltration in a peritonitis model, further enhancing the therapeutic effect of HUC-MSCs [6, Supplementary Fig. 6]. Overall, KYNA, an IDO1 metabolite, was able to activate AhR signaling, leading to increased TSG-6 production in HUC-MSCs [6].
Figure [1]
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Figure [2]
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Figure [3]
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Figure [4]
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Figure [5]
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Figure [6]
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Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the IDO1 target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.
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