بررسي اثر ايندولامين 2 و 3 دي اكسيژناز در دور زدن پاسخ هاي مهار كننده نقاط وارسي: بروز شده

Metabolic alterations occur commonly in tumor cells as a way to adapt available energetic sources for their proliferation, survival an‎d resistance. Indoleamine 2,3-dioxygenase 1 (IDO1) is an intracellular enzyme cata lyzing tryptophan degradation into kynurenine. IDO1 expression shows a rise in the stroma of many types of human cancers, an‎d it provides a negative feedback mechanism for cancer evasion from immunosurveillance. Upregulation of IDO1 correlates with cancer aggression, poor prognosis an‎d shortened patient survival. The increased activity of this endogenous checkpoint impairs effector T cell function, increases regulatory T cell (Treg) population an‎d induces immune tolerance, so its inhibition potentiates anti-tumor immune responses an‎d reshapes immunogenic state of tumor microenvironment (TME) presumably through normalizing effector T cell activity. A point is that the expression of this immunoregulatory marker is upregulated after immune checkpoint inhibitor (ICI) therapy, an‎d that it has inducible effect on expression of other checkpoints. These are indicative of the importance of IDO1 as an attractive immunotherapeutic target an‎d rationalizing combination of IDO1 in hibitors with ICI drugs in patients with advanced solid cancers. In this review, we aimed to discuss about the impact of IDO1 on tumor immune ecosystem, an‎d the IDO1-mediated bypass of ICI therapy. The efficacy of IDO1 inhibitor therapy in combination with ICIs in advanced/metastatic solid tumors is also a focus of this paper.

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