This product consists of a polyclonal population of IDO1 knockout TE1 cells generated by CRISPR/Cas9-mediated gene disruption. The edited pool retains the heterogeneous background of the parental TE1 line while lacking functional IDO1 expression, providing a robust loss-of-function model for studying tryptophan catabolism and immune regulation. The polyclonal format avoids clonal selection biases and is suitable for experiments where population-level responses to IDO1 ablation are required.
The TE1 cell line is a human esophageal squamous cell carcinoma model derived from a well-differentiated esophageal squamous epithelial carcinoma. It is widely employed in cancer biology to investigate signaling pathways, drug responses, and tumor?Cimmune interactions characteristic of esophageal malignancies. The epithelial origin and malignant phenotype of TE1 make it an appropriate host for interrogating IDO1-mediated mechanisms in a tumor-intrinsic context.
IDO1 encodes indoleamine 2,3-dioxygenase 1, a rate?limiting enzyme that catalyzes the oxidative cleavage of tryptophan to produce kynurenine. This reaction depletes local tryptophan and generates bioactive kynurenine metabolites that activate the aryl hydrocarbon receptor (AhR), ultimately driving effector T?cell anergy, regulatory T?cell (Treg) expansion, and natural killer (NK) cell inhibition. IDO1 expression is potently induced by pro?inflammatory and immunoregulatory signals including interferon??? (IFN???), interleukin?1?? (IL?1??), tumor necrosis factor??? (TNF???), and transforming growth factor??? (TGF???), and is further modulated by CTLA?4 signaling. The enzyme physically interacts with cytochrome b5 and Hsp90, and functions alongside enzymes such as tryptophan 2,3?dioxygenase (TDO2) to shape the kynurenine pathway. Downstream metabolites including kynurenic acid and quinolinic acid reinforce immunosuppressive circuits through AhR engagement.
In esophageal squamous cell carcinoma, IDO1 expression contributes to an immunosuppressive tumor microenvironment that facilitates immune escape. Disrupting IDO1 in the TE1 background allows researchers to dissect how tumor?derived tryptophan metabolism influences T?cell function, Treg induction, and NK cell activity within a relevant carcinoma model. The knockout helps separate tumor?cell?intrinsic effects of IDO1 from those of host immune cells, and can be paired with co?culture systems to evaluate how loss of IDO1 alters the reciprocal crosstalk between carcinoma cells and immune effectors.
This knockout cell population is well?suited for investigating mechanisms of tumor immune evasion, screening IDO1?targeted inhibitors, and evaluating immunotherapy resistance in a high?throughput format. Experimental validation can be performed via western blotting for IDO1 protein, RT?qPCR for IDO1 mRNA, HPLC? or ELISA?based quantification of kynurenine production, and T?cell suppression co?culture assays. Additionally, flow cytometry can monitor changes in Treg induction, and AhR activation reporter assays can link IDO1 loss to altered AhR signaling. For further information, please contact Ascent Research.
