Vitamin D helps calm inflammation in certain immune cells by stopping a specific switch in the cell’s DNA from turning on a molecule that causes inflammation.
See the scientific wording
Vitamin D suppresses microRNA-155 transcription in macrophages by enabling vitamin D receptor signaling to block NF-κB binding to a specific DNA element in the first intron of the bic gene, thereby exerting an anti-inflammatory effect.
Correlational — new studies may shift this
ObservationalOne low-scoring study links this claim to the outcome, but causation is not established.
What the research says
1 study reviewedSupporting (1)
Case-Control StudyAnimal2013
Vitamin D helps calm down inflammation in immune cells by blocking a specific DNA switch that would otherwise turn on a trouble-making molecule called miR-155. This switch is right inside a gene called bic, and vitamin D stops a protein (NF-κB) from activating it.
Contradicting (0)
No contradicting studies found yet
That doesn't mean it's settled — it just means no study has tested the opposite.
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Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting study
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Vitamin D helps calm inflammation in certain immune cells by stopping a specific switch in the cell’s DNA from turning on a molecule that causes inflammation.
Evidence from Studies
Supporting (1)
Community contributions welcome
1,25-Dihydroxyvitamin D Promotes Negative Feedback Regulation of TLR Signaling via Targeting MicroRNA-155–SOCS1 in Macrophages
Vitamin D helps calm down inflammation in immune cells by blocking a specific DNA switch that would otherwise turn on a trouble-making molecule called miR-155. This switch is right inside a gene called bic, and vitamin D stops a protein (NF-κB) from activating it.
1 study stuck in processing — a maintainer can requeue it.
Contradicting (0)
Community contributions welcome
1 study has been processing far longer than a normal run. The pipeline may be stuck — a maintainer can requeue it, and the results will appear here once it finishes.
Score Breakdown
No multi-axis breakdown available yet. The overall Pro / Against score above is the best signal.
- No clinical evidence is available; the score reflects mechanistic plausibility only.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
Systematic Review of Vitamin D Receptor Binding to Bic Gene Intronic Elements and MicroRNA-155 Suppression in Macrophages
Systematic review and meta-analysis of all peer-reviewed in vitro and animal studies examining vitamin D receptor binding to the first intron of the bic gene, NF-κB displacement, and microRNA-155 downregulation in macrophages.
Randomized Controlled Trial of Vitamin D Supplementation on Macrophage MicroRNA-155 and Inflammatory Markers in Humans with Chronic Inflammation
Double-blind, placebo-controlled trial in humans with chronic inflammatory conditions, administering vitamin D vs. placebo, measuring macrophage microRNA-155 levels, NF-κB binding, and bic gene intronic activity via biopsy or isolated monocytes over 12 weeks.
Prospective Cohort Study of Vitamin D Levels and Macrophage MicroRNA-155 Expression in Individuals with Varying Inflammatory Status
Longitudinal cohort tracking serum vitamin D levels, peripheral blood monocyte-derived macrophage microRNA-155 expression, and inflammatory biomarkers in 500 individuals over 2 years.
In Vitro Study Demonstrating Vitamin D Receptor Binding to Bic Gene First Intron and NF-κB Displacement in Human Macrophage Cell Lines
Human macrophage cell line experiments using chromatin immunoprecipitation (ChIP) and luciferase reporter assays to confirm vitamin D receptor binding to the first intron of the bic gene and inhibition of NF-κB binding upon vitamin D exposure.
Animal Model Study of Vitamin D-Induced Suppression of MicroRNA-155 via Bic Gene Regulation in Macrophages of Inflamed Mice
C57BL/6 mice with induced macrophage inflammation treated with vitamin D or vehicle; analysis of macrophage bic gene intronic binding, NF-κB occupancy, microRNA-155 levels, and inflammatory cytokines over 4 weeks.