Component
Mouse T-cell proliferation under tryptophan limitation or IDO exposure
Context-specific entity; species, compartment and exposure are stated on each claim.
3 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 acts on it
Donor mouse T cells lacking GCN2 still responded to IDO-mediated suppression in graft-versus-host disease experiments.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse allogeneic transplantation and donor T-cell genetics.
- limitations
- The authors favor metabolite-mediated suppression; it does not prove which single metabolite explains all models.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- In a transplant model, IDO suppression also persisted without GCN2.
- primary_references
- Inducing the tryptophan catabolic pathway, indoleamine 2,3-dioxygenase (IDO), for suppression of graft-versus-host disease (GVHD) lethality. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19828695/ · DOI 10.1182/blood-2009-06-227587
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 394–400
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse allogeneic transplantation and donor T-cell genetics. · source_derived_draft · unverified_draft
## tryptophan-gcn2-gvhd In a transplant model, IDO suppression also persisted without GCN2. Donor mouse T cells lacking GCN2 still responded to IDO-mediated suppression in graft-versus-host disease experiments. Model: Mouse allogeneic transplantation and donor T-cell genetics. Limitations: The authors favor metabolite-mediated suppression; it does not prove which single metabolite explains all models. Evidence access: Primary abstract Inducing the tryptophan catabolic pathway, indoleamine 2,3-dioxygenase (IDO), for suppression of graft-versus-host disease (GVHD) lethality. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19828695/ · DOI 10.1182/blood-2009-06-227587
Complete structured claim and evidenceGCN2-deficient mouse CD8 T cells still failed to proliferate under limiting tryptophan, arginine, leucine, lysine or asparagine in the 2016 study.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Gcn2-deficient mice crossed to TCR-transgenic backgrounds; defined amino-acid limitation.
- limitations
- Not identical to every IDO-dendritic-cell preparation; the authors explicitly challenge the earlier necessity model.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Another study found the division block persisted without that sensor.
- primary_references
- Stress Kinase GCN2 Controls the Proliferative Fitness and Trafficking of Cytotoxic T Cells Independent of Environmental Amino Acid Sensing. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27880901/ · DOI 10.1016/j.celrep.2016.10.079
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 378–384
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Gcn2-deficient mice crossed to TCR-transgenic backgrounds; defined amino-acid limitation. · source_derived_draft · unverified_draft
## tryptophan-gcn2-not-required Another study found the division block persisted without that sensor. GCN2-deficient mouse CD8 T cells still failed to proliferate under limiting tryptophan, arginine, leucine, lysine or asparagine in the 2016 study. Model: Gcn2-deficient mice crossed to TCR-transgenic backgrounds; defined amino-acid limitation. Limitations: Not identical to every IDO-dendritic-cell preparation; the authors explicitly challenge the earlier necessity model. Evidence access: Primary abstract Stress Kinase GCN2 Controls the Proliferative Fitness and Trafficking of Cytotoxic T Cells Independent of Environmental Amino Acid Sensing. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27880901/ · DOI 10.1016/j.celrep.2016.10.079
Complete structured claim and evidenceGCN2-deficient mouse T cells resisted suppression and anergy imposed by IDO-expressing dendritic cells in the 2005 study.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse Gcn2 knockout, IDO-positive plasmacytoid/tumor-draining dendritic-cell experiments.
- limitations
- A later genetic study reports arrest without GCN2; necessity is not universal across the available evidence.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- One study found this nutrient-stress sensor necessary for suppression.
- primary_references
- GCN2 kinase in T cells mediates proliferative arrest and anergy induction in response to indoleamine 2,3-dioxygenase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15894280/ · DOI 10.1016/j.immuni.2005.03.013
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 370–376
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Gcn2 knockout, IDO-positive plasmacytoid/tumor-draining dendritic-cell experiments. · source_derived_draft · unverified_draft
## tryptophan-gcn2-required One study found this nutrient-stress sensor necessary for suppression. GCN2-deficient mouse T cells resisted suppression and anergy imposed by IDO-expressing dendritic cells in the 2005 study. Model: Mouse Gcn2 knockout, IDO-positive plasmacytoid/tumor-draining dendritic-cell experiments. Limitations: A later genetic study reports arrest without GCN2; necessity is not universal across the available evidence. Evidence access: Primary abstract GCN2 kinase in T cells mediates proliferative arrest and anergy induction in response to indoleamine 2,3-dioxygenase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15894280/ · DOI 10.1016/j.immuni.2005.03.013
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.