Component
Experimental autoimmune encephalomyelitis
Experimental autoimmune encephalomyelitis. Species, exposure and limitations are retained in each linked claim.
1 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.
Where it participates (unsigned role)
Immune cells synthesize GABA and have the machinery for GABA catabolism, antigen-presenting cells express functional GABA receptors and respond electrophysiologically to GABA, thus the immune system harbors all of the necessary constituents for GABA signaling and GABA itself may function as a paracrine or autocrine factor, increasing GABAergic activity ameliorates ongoing paralysis in experimental autoimmune encephalomyelitis via inhibition of inflammation, and GABAergic agents act directly on antigen-presenting cells decreasing MAPK signals and diminishing subsequent adaptive inflammatory responses to myelin proteins.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/gaba-research/20133656.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd", "start_char": 0, "end_char": 896, "text_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd"}
- experimental_model
- Demonstration of GABA synthesis and catabolism machinery in immune cells with electrophysiology and an autoimmune disease model
- exposure
- Increasing GABAergic activity in established experimental autoimmune encephalomyelitis
- limitations
- The disease effect is on ongoing paralysis rather than prevention. The assignment to antigen-presenting cells rests on direct effects measured on those cells.
- 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
- The immune system has the whole apparatus to make and break down this transmitter, and uses it on itself.
- primary_references
- [gb-p20133656] Inhibitory role for GABA in autoimmune inflammation. (2010). https://pubmed.ncbi.nlm.nih.gov/20133656/ DOI: 10.1073/pnas.0915139107
- tissue_or_cell_type
- Antigen-presenting cell and central nervous system
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Demonstration of GABA synthesis and catabolism machinery in immune cells with electrophysiology and an autoimmune disease model · source_derived_draft · unverified_draft
### gb-immune-cells-make-their-own-gaba Immune cells synthesize GABA and have the machinery for GABA catabolism, antigen-presenting cells express functional GABA receptors and respond electrophysiologically to GABA, thus the immune system harbors all of the necessary constituents for GABA signaling and GABA itself may function as a paracrine or autocrine factor, increasing GABAergic activity ameliorates ongoing paralysis in experimental autoimmune encephalomyelitis via inhibition of inflammation, and GABAergic agents act directly on antigen-presenting cells decreasing MAPK signals and diminishing subsequent adaptive inflammatory responses to myelin proteins. 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: The immune system has the whole apparatus to make and break down this transmitter, and uses it on itself. organism: Mouse tissue_or_cell_type: Antigen-presenting cell and central nervous system experimental_model: Demonstration of GABA synthesis and catabolism machinery in immune cells with electrophysiology and an autoimmune disease model limitations: The disease effect is on ongoing paralysis rather than prevention. The assignment to antigen-presenting cells rests on direct effects measured on those cells. exposure: Increasing GABAergic activity in established experimental autoimmune encephalomyelitis evidence_span: {"source_cache": "artifacts/gaba-research/20133656.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd", "start_char": 0, "end_char": 896, "text_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd"} [gb-p20133656] Inhibitory role for GABA in autoimmune inflammation. (2010). https://pubmed.ncbi.nlm.nih.gov/20133656/ DOI: 10.1073/pnas.0915139107
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.