IL4I1 (Interleukin 4 Induced 1)

Myeloid cells exhibited expression of immunomodulatory genes (RUNX3, DDIT4, IL4I1), and malignant T-cells expressed exhaustion-associated markers (CXCL13, SOCS3, F2R, ETV1), as opposed to AD and healthy control samples. Thus, our results provide a novel insight into the immune-stroma crosstalk in the tissue microenvironment of early-stage MF vs. AD skin lesions.

Branched-chain amino acid metabolism and IL4I1 are pivotal in the progression of ccRCC. AS classification and the AIS score present a robust framework for personalized treatment strategies, while IL4I1 shows potential as a novel therapeutic target to enhance treatment efficacy.

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.

Consequently, IL4I1 emerges as a significant prognostic biomarker and a promising therapeutic target, driving ongoing development of targeted inhibitors. This review comprehensively synthesizes the structural, functional, and clinical landscape of IL4I1, highlighting its therapeutic potential.

Overall, we demonstrate the key role of IL4I1 in TAM-mediated immune escape of melanoma. As most human tumors contain TAMs expressing IL4I1, our results may have implications for cancer immunotherapy.

This study suggests that IDO1 and IL4I1, which are involved in tumor metabolism, may play an important role in regulating TAMs immune infiltration in breast cancer. Therefore, IDO1 and IL4I1 are potential therapeutic targets for breast cancer.

PIM blockade attenuated TAM-dependent eosinophil chemoattraction, extracellular matrix remodeling, angiogenesis and regulatory T-cell development. Taken together, our study highlights the role of PIMs in the regulation of pathogenic TAM functions in cHL, further supporting the rationale of PIM targeting in this disease.

A triple therapy combining CH-223191, ferroptosis inducer (Imidazole ketone erastin or RSL3), and anti-PD-1 agent demonstrates superior efficacy and safety in vivo. Together, our findings demonstrate that IL4I1⁺ TAMs and TDO2⁺ myCAFs synergistically establish an immunosuppressive, ferroptosis-resistant niche via AhR signaling in solid predominant LUAD and offer promising therapeutic strategies to reprogram the tumor microenvironment.

This study clarified a specific signature associated with fatty acid metabolism, specifically FASN, which is connected to both the initiation and progression of CESC. Furthermore, FASN may serve as a prognostic marker for individuals diagnosed with CESC, thus providing fresh insights for the formulation of clinical treatment strategies.

Tryptophan-kynurenine enzymes shape the immune landscape of EC in a subtype-specific manner. High IDO1 was linked to favourable outcomes in p53mut and NSMP cases, whereas TDO2 predicted poor prognosis. The CD163:CD8 ratio emerged as an independent marker of poor survival. These findings support therapeutic strategies combining dual IDO1/TDO2 inhibition or targeting the IL4I1- aryl hydrocarbon receptor (AhR) axis to enhance immunotherapy efficacy in EC.

IELs exhibit a cytotoxic T-cell phenotype and were found to be CD3+, CD8+, CD103+, TCR beta+, and LAIR1+ in the small intestine control. Increased numbers of LAIR1+ IELs and lamina propria immune cells characterize CD.