Component
Human interleukin-4-induced protein 1 / IL4I1
Context-specific entity; species, compartment and exposure are stated on each claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
IDO1 inhibitors did not block IL4I1 in the study, leaving an alternative route to AHR activation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Cancer-mechanism experiments.
- limitations
- An explanation proposed for clinical trial failure, not proof that IL4I1 caused failure in every patient.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Blocking one enzyme does not necessarily close a parallel route.
- primary_references
- IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 458–464
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-mechanism experiments. · source_derived_draft · unverified_draft
## tryptophan-ido-drug-bypass Blocking one enzyme does not necessarily close a parallel route. IDO1 inhibitors did not block IL4I1 in the study, leaving an alternative route to AHR activation. Model: Cancer-mechanism experiments. Limitations: An explanation proposed for clinical trial failure, not proof that IL4I1 caused failure in every patient. Evidence access: Primary abstract IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038
Complete structured claim and evidenceIL4I1 generated indole metabolites and kynurenic acid that activated AHR in the cancer study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human cancer/biochemical work with separate mouse CLL experiments.
- limitations
- This abstract groups several products; their individual concentrations and relative causal contributions are not resolved here.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Another enzyme can feed the same receptor through different metabolites.
- primary_references
- IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 450–456
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cancer/biochemical work with separate mouse CLL experiments. · source_derived_draft · unverified_draft
## tryptophan-il4i1-route Another enzyme can feed the same receptor through different metabolites. IL4I1 generated indole metabolites and kynurenic acid that activated AHR in the cancer study. Model: Human cancer/biochemical work with separate mouse CLL experiments. Limitations: This abstract groups several products; their individual concentrations and relative causal contributions are not resolved here. Evidence access: Primary abstract IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32818467/ · DOI 10.1016/j.cell.2020.07.038
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.