Human activated T-cell proliferation: molecular mechanisms & dependencies

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.

Human evidence only

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.

Recorded relationships

What acts on it

Human T cells activated without tryptophan arrested in mid-G1 while retaining early activation and some protein synthesis.
L-Tryptophan → Human activated T-cell proliferation source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary full text, cell-cycle results
experimental_model
Human purified T cells activated with anti-CD3/CD28.
limitations
Not synonymous with immediate cell death or complete cessation of protein synthesis.
nutrient_topic
Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
plain_language
Cells could begin activation but could not complete the division program.
primary_references
Inhibition of T cell proliferation by macrophage tryptophan catabolism. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10224276/ · DOI 10.1084/jem.189.9.1363
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 354–360
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human purified T cells activated with anti-CD3/CD28. · source_derived_draft · unverified_draft
## tryptophan-tcell-arrest Cells could begin activation but could not complete the division program. Human T cells activated without tryptophan arrested in mid-G1 while retaining early activation and some protein synthesis. Model: Human purified T cells activated with anti-CD3/CD28. Limitations: Not synonymous with immediate cell death or complete cessation of protein synthesis. Evidence access: Primary full text, cell-cycle results Inhibition of T cell proliferation by macrophage tryptophan catabolism. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10224276/ · DOI 10.1084/jem.189.9.1363
Complete structured claim and evidence
After tryptophan-sensitive arrest, human T cells required renewed T-cell-receptor signaling as well as tryptophan to resume division.
L-Tryptophan → Human activated T-cell proliferation source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary full text, TCR-dependence results
experimental_model
Human T-cell withdrawal, add-back and receptor-restimulation experiments.
limitations
A cell-cycle checkpoint experiment, not a general human supplementation rule.
nutrient_topic
Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
plain_language
Replacing the nutrient alone did not restore the lost activation commitment.
primary_references
Inhibition of T cell proliferation by macrophage tryptophan catabolism. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10224276/ · DOI 10.1084/jem.189.9.1363
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 362–368
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human T-cell withdrawal, add-back and receptor-restimulation experiments. · source_derived_draft · unverified_draft
## tryptophan-tcell-restimulation Replacing the nutrient alone did not restore the lost activation commitment. After tryptophan-sensitive arrest, human T cells required renewed T-cell-receptor signaling as well as tryptophan to resume division. Model: Human T-cell withdrawal, add-back and receptor-restimulation experiments. Limitations: A cell-cycle checkpoint experiment, not a general human supplementation rule. Evidence access: Primary full text, TCR-dependence results Inhibition of T cell proliferation by macrophage tryptophan catabolism. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10224276/ · DOI 10.1084/jem.189.9.1363
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.

Human activated T-cell proliferation