B cell: 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 it acts on

We identify the metabolite and neurotransmitter GABA as a candidate signalling molecule synthesized and secreted by activated B cells and plasma cells, B cell-derived GABA promotes monocyte differentiation into anti-inflammatory macrophages that secrete interleukin-10 and inhibit CD8-positive T cell killer function, and in mice B cell deficiency or B cell-specific inactivation of the GABA-generating enzyme GAD67 enhances anti-tumour responses.
B cell → Gamma-aminobutyric acid source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/gaba-research/34732892.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b", "start_char": 0, "end_char": 878, "text_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b"}
experimental_model
Identification of a metabolite secreted by activated B cells, with monocyte differentiation and two genetic tests in mice
exposure
B cell-derived GABA, with B cell deficiency and B cell-specific inactivation of the GABA-generating enzyme GAD67
limitations
The B cell-specific enzyme deletion is what makes the source assignment strong. The enzyme deleted is GAD67, not the GAD65 that is the diabetes autoantigen.
nutrient_topic
GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
organism
Mouse
plain_language
B cells release this molecule into a tumour, where it turns arriving monocytes into cells that shut down the killers.
primary_references
[gb-p34732892] B cell-derived GABA elicits IL-10+ macrophages to limit anti-tumour immunity. (2021). https://pubmed.ncbi.nlm.nih.gov/34732892/ DOI: 10.1038/s41586-021-04082-1
tissue_or_cell_type
B cell, monocyte and tumour
GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 599–610
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Identification of a metabolite secreted by activated B cells, with monocyte differentiation and two genetic tests in mice · source_derived_draft · unverified_draft
### gb-b-cells-secrete-gaba-that-shields-tumours We identify the metabolite and neurotransmitter GABA as a candidate signalling molecule synthesized and secreted by activated B cells and plasma cells, B cell-derived GABA promotes monocyte differentiation into anti-inflammatory macrophages that secrete interleukin-10 and inhibit CD8-positive T cell killer function, and in mice B cell deficiency or B cell-specific inactivation of the GABA-generating enzyme GAD67 enhances anti-tumour responses. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: B cells release this molecule into a tumour, where it turns arriving monocytes into cells that shut down the killers. organism: Mouse tissue_or_cell_type: B cell, monocyte and tumour experimental_model: Identification of a metabolite secreted by activated B cells, with monocyte differentiation and two genetic tests in mice limitations: The B cell-specific enzyme deletion is what makes the source assignment strong. The enzyme deleted is GAD67, not the GAD65 that is the diabetes autoantigen. exposure: B cell-derived GABA, with B cell deficiency and B cell-specific inactivation of the GABA-generating enzyme GAD67 evidence_span: {"source_cache": "artifacts/gaba-research/34732892.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b", "start_char": 0, "end_char": 878, "text_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b"} [gb-p34732892] B cell-derived GABA elicits IL-10+ macrophages to limit anti-tumour immunity. (2021). https://pubmed.ncbi.nlm.nih.gov/34732892/ DOI: 10.1038/s41586-021-04082-1
Complete structured claim and evidence

Where it participates (unsigned role)

Dendritic-cell-derived RA conferred gut tropism on activated B cells.
All-trans-retinoic acid → B-cell gut homing source_derived_draftungraded
Experimental context and source evidence
evidence_locator
Abstract
experimental_model
Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice.
exposure
Gut dendritic-cell-derived RA
limitations
Gut tropism alone is not IgA secretion.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Mus musculus
plain_language
RA helps route antibody-producing cell precursors to the intestine.
primary_references
[va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
tissue_or_cell_type
B-cell cultures
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1214–1225
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. · source_derived_draft · unverified_draft
### va-sig-ra-b-cell-homing Dendritic-cell-derived RA conferred gut tropism on activated B cells. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RA helps route antibody-producing cell precursors to the intestine. organism: Mus musculus tissue_or_cell_type: B-cell cultures experimental_model: Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. limitations: Gut tropism alone is not IgA secretion. evidence_locator: Abstract exposure: Gut dendritic-cell-derived RA [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
Complete structured claim and evidence
RA alone was insufficient for IgA secretion but cooperated with IL-6 or IL-5 to induce it.
All-trans-retinoic acid → Immunoglobulin A source_derived_draftungraded
Experimental context and source evidence
evidence_locator
Abstract
experimental_model
Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice.
exposure
RA with IL-6 or IL-5
limitations
Cannot generalize to every IgA-switching pathway.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Mus musculus
plain_language
IgA output required additional immune signals in this experiment.
primary_references
[va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
tissue_or_cell_type
B-cell cultures
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1227–1238
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. · source_derived_draft · unverified_draft
### va-sig-ra-cytokine-iga RA alone was insufficient for IgA secretion but cooperated with IL-6 or IL-5 to induce it. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: IgA output required additional immune signals in this experiment. organism: Mus musculus tissue_or_cell_type: B-cell cultures experimental_model: Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. limitations: Cannot generalize to every IgA-switching pathway. evidence_locator: Abstract exposure: RA with IL-6 or IL-5 [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
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.

B cell