IDO1 (Indoleamine 2,3-dioxygenase 1)

Furthermore, PDT-induced tumor hypoxia activated an indoleamine 2,3-dioxygenase-1 (IDO-1) inhibitor prodrug, directly mitigating regulatory T cell expansion triggered by immunogenic cell death. By integration of broad-spectrum antigen presentation with hypoxia-responsive immunosuppression reversal, this dual-modality nanovaccine achieved potent suppression of both primary and distant tumors.

Its capability to overcome tumor resistance and the underlying mechanism were further investigated in a well-established tumor model. Our findings highlight the cooperative role of STING activation and IDO1 blockade within cDC1s and introduce an integrated drug delivery system to combat immune tolerance in cancer therapy.

This review highlights the multifaceted role of IL4I1 within the TME, focusing on its immune regulatory function and anti-ferroptotic function. By exploring IL4I1's function in regulating different immune cell subsets and new role in promoting tumor resistance to ferroptosis, we discuss the major unanswered questions about how IL4I1 regulates tumor immunity, and propose the significance of developing targeted therapies that inhibit IL4I1, potentially in combination with inhibitors targeting IDO1 or immune checkpoints, to enhance antitumor immunity and improve clinical outcomes of cancer patients.

This article focuses on the interaction mechanism of cells and molecules in the tumor immune microenvironment (TiME) involved in the occurrence and development of TC and analyzes its potential value as a therapeutic target. In addition, the latest clinical trials related to immunotherapy for TC are summarized.

P1, N=16, Terminated, Rutgers, The State University of New Jersey | Active, not recruiting --> Terminated; accrual goal met

With respect to drug response, PRKD1-high HCC cases exhibited increased predicted sensitivity to multiple tyrosine kinase inhibitors (TKIs), while in vitro PRKD1 knockdown reduced sorafenib sensitivity, and sorafenib treatment suppressed both PRKD1 and p-ERK1/2 levels. Collectively, our findings identify PRKD1 as a multifaceted contributor to HCC progression, immune microenvironment modulation, and TKI responsiveness. These results highlight PRKD1 as a promising therapeutic target warranting further mechanistic and translational investigation.

In addition, the immunosuppressive microenvironment exacerbated by postoperative hypoxia is degraded via the cooperation of NLG919, which blocks the IDO-1 signaling pathway and CaCO3, which consumes lactic acid. Based on these improvements, well-designed MOFs effectively inhibit bilateral tumor growth/metastasis and offer a successful paradigm for improving the overall prognosis of HIFU.

The IDO family plays a multifaceted and context-dependent role in various diseases through the kynurenine pathway, making it a promising target for diagnostic biomarkers and therapeutic intervention. Future research should focus on optimizing multi-target inhibitors, developing innovative delivery systems, establishing biomarker-guided precision medicine strategies, and exploring non-enzymatic functions and downstream signaling networks of the IDO family. These efforts will help overcome the limitations of current therapies and provide new treatment paradigms for refractory diseases related to immune metabolic disorders.

We investigated the impact of the CHOP regimen and its components (cyclophosphamide (CTX), doxorubicin, vincristine, and prednisolone) on the dynamics of MDSC accumulation and the associated changes in immune cell profiles in the peripheral blood and spleen of healthy and lymphosarcoma RLS40-bearing CBA mice. Thus, our results highlight CTX's central role in CHOP-induced MDSC expansion. The structure-dependent duality of triterpenoids, countering (GLZ) or promoting (FM) MDSC expansion, offers therapeutic potential for pathologies ranging from chemotherapy-induced side effects to autoimmunity.

This study establishes the first H&E-based Pathomics framework for quantifying CAFs infiltration in RCC, providing a cost-effective and non-invasive tool for preliminary risk stratification. The model's strong correlation with collagen features and its ability to reveal underlying molecular mechanisms highlight its potential for potential value in understanding the stromal microenvironment, though further external validation is required for clinical translation.

Our findings establish that IDO1 modulates macrophage immunometabolism to foster a pro-inflammatory intrahepatic milieu, thereby aggravating hepatocyte mitochondrial oxidative stress and death in early AILI. This reveals IDO1 as a key regulator of immune-metabolic crosstalk in AILI and underscores its potential both as a biomarker and a promising therapeutic target.

Deep learning-derived CTBC metrics, especially VAT/SAT ratio, enhance prognostic stratification beyond TNM staging in locally advanced gastric cancer. This ratio captures a systemic and tumor-level immunometabolic phenotype marked by mitochondrial dysfunction and immune suppression. Our findings highlight VAT/SAT as a noninvasive, clinically actionable biomarker to guide personalized therapy and risk-adapted algorithm in gastric cancer management.