Component

Vitamin D 1-alpha-hydroxylase / CYP27B1

Independent biological entity. Read linked claims for experimental scope and context.

14 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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

  1. Human CYP27B1 1alpha-hydroxylated 25-hydroxyvitamin D2 in phospholipid vesicles; low-substrate catalytic efficiency was similar to that measured for calcifediol.

    Vitamin D 1-alpha-hydroxylase / CYP27B1 → 1-alpha,25-Dihydroxyvitamin D2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary Tables 3-5, Figure 6A and Experimental procedures; full text retrieved.
    experimental_model
    Partially purified human CYP27B1 membrane assay
    exposure
    5-40 nM CYP27B1; 15 micromolar FDX1, 0.4 micromolar FDXR, 50 micromolar NADPH; 2 min at 37 C. Table 5/Figure 6A.
    limitations
    D2 kinetic data came from one experiment; results do not establish human dosing equivalence.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens proteins
    plain_language
    CYP27B1 completes activation of the D2 precursor.
    primary_references
    [tang2012] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles. (2012). https://pubmed.ncbi.nlm.nih.gov/22862690/ DOI: 10.1111/j.1742-4658.2012.08736.x
    tissue_or_cell_type
    reconstituted inner-mitochondrial-membrane model

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 437–450

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified human CYP27B1 membrane assay · source_derived_draft · unverified_draft

    ### vd-act-cyp27b1-d2 Human CYP27B1 1alpha-hydroxylated 25-hydroxyvitamin D2 in phospholipid vesicles; low-substrate catalytic efficiency was similar to that measured for calcifediol. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CYP27B1 completes activation of the D2 precursor. organism: Homo sapiens proteins tissue_or_cell_type: reconstituted inner-mitochondrial-membrane model experimental_model: Partially purified human CYP27B1 membrane assay limitations: D2 kinetic data came from one experiment; results do not establish human dosing equivalence. exposure: 5-40 nM CYP27B1; 15 micromolar FDX1, 0.4 micromolar FDXR, 50 micromolar NADPH; 2 min at 37 C. Table 5/Figure 6A. cross_nutrient: false evidence_location: Primary Tables 3-5, Figure 6A and Experimental procedures; full text retrieved. nutrient: Vitamin D2 and D3 [tang2012] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles. (2012). https://pubmed.ncbi.nlm.nih.gov/22862690/ DOI: 10.1111/j.1742-4658.2012.08736.x
    Complete structured claim and evidence

  2. Recombinant human CYP27B1 converts calcifediol to calcitriol by 1-alpha-hydroxylation in reconstituted enzyme systems.

    Vitamin D 1-alpha-hydroxylase / CYP27B1 → Calcitriol source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Recombinant human CYP27B1 expressed in bacteria and reconstituted with phospholipids and electron-transfer partners
    limitations
    Activity requires electron-transfer support; this assay does not measure endocrine flux in an intact kidney.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens enzyme
    plain_language
    CYP27B1 activates the vitamin D precursor.
    primary_references
    [tang2012cyp27b1] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles (2012). https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2012.08736.x DOI: 10.1111/j.1742-4658.2012.08736.x
    research_relationship_category
    biochemical_reaction
    tissue_or_cell_type
    Reconstituted membrane system
    transport_or_reaction_direction
    forward

    Calcium: mechanism-first literature curation (2026-09-17) · lines 349–360

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human CYP27B1 expressed in bacteria and reconstituted with phospholipids and electron-transfer partners · source_derived_draft · unverified_draft

    ### cyp27b1-produces-calcitriol Recombinant human CYP27B1 converts calcifediol to calcitriol by 1-alpha-hydroxylation in reconstituted enzyme systems. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: CYP27B1 activates the vitamin D precursor. organism: Homo sapiens enzyme tissue_or_cell_type: Reconstituted membrane system experimental_model: Recombinant human CYP27B1 expressed in bacteria and reconstituted with phospholipids and electron-transfer partners limitations: Activity requires electron-transfer support; this assay does not measure endocrine flux in an intact kidney. research_relationship_category: biochemical_reaction transport_or_reaction_direction: forward [tang2012cyp27b1] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles (2012). https://febs.onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2012.08736.x DOI: 10.1111/j.1742-4658.2012.08736.x
    Complete structured claim and evidence

What acts on it

  1. Human adrenodoxin supported CYP27B1 activity in reconstituted vesicles; varying adrenodoxin changed apparent kinetic parameters for calcifediol hydroxylation.

    Human adrenodoxin / FDX1 → Vitamin D 1-alpha-hydroxylase / CYP27B1 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Primary Tables 3-5, Figure 6A and Experimental procedures; full text retrieved.
    experimental_model
    Human CYP27B1/FDX1/FDXR kinetic reconstitution
    exposure
    FDX1 1-30 micromolar; 2-min incubations with calcifediol; Table 4.
    limitations
    The experiment varies intact FDX1, not dietary iron. Reciprocal changes of apparent Km and turnover prevent interpreting FDX1 level as a universal limiting factor.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens proteins
    plain_language
    An iron-sulfur electron carrier supports the final D3 activation step.
    primary_references
    [tang2012] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles. (2012). https://pubmed.ncbi.nlm.nih.gov/22862690/ DOI: 10.1111/j.1742-4658.2012.08736.x
    tissue_or_cell_type
    reconstituted mitochondrial membrane

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 452–465

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CYP27B1/FDX1/FDXR kinetic reconstitution · source_derived_draft · unverified_draft

    ### vd-act-fdx1-cyp27b1 Human adrenodoxin supported CYP27B1 activity in reconstituted vesicles; varying adrenodoxin changed apparent kinetic parameters for calcifediol hydroxylation. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An iron-sulfur electron carrier supports the final D3 activation step. organism: Homo sapiens proteins tissue_or_cell_type: reconstituted mitochondrial membrane experimental_model: Human CYP27B1/FDX1/FDXR kinetic reconstitution limitations: The experiment varies intact FDX1, not dietary iron. Reciprocal changes of apparent Km and turnover prevent interpreting FDX1 level as a universal limiting factor. exposure: FDX1 1-30 micromolar; 2-min incubations with calcifediol; Table 4. cross_nutrient: true evidence_location: Primary Tables 3-5, Figure 6A and Experimental procedures; full text retrieved. nutrient: Vitamin D2 and D3 [tang2012] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles. (2012). https://pubmed.ncbi.nlm.nih.gov/22862690/ DOI: 10.1111/j.1742-4658.2012.08736.x
    Complete structured claim and evidence

  2. Recombinant FGF23 lowers renal CYP27B1 mRNA before the fall in serum phosphate.

    Fibroblast growth factor 23 / FGF23 → Vitamin D 1-alpha-hydroxylase / CYP27B1 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Recombinant FGF23 injections in normal and parathyroidectomized rodents
    limitations
    Injection study; transcript change is not direct enzyme inhibition.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus; Rattus norvegicus
    plain_language
    FGF23 restrains a vitamin D activation enzyme.
    primary_references
    [shimada2004injection] FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis (2004). https://pubmed.ncbi.nlm.nih.gov/15040831/ DOI: 10.1359/JBMR.0301264
    tissue_or_cell_type
    Kidney

    Calcium: mechanism-first literature curation (2026-09-17) · lines 91–100

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant FGF23 injections in normal and parathyroidectomized rodents · source_derived_draft · unverified_draft

    ### fgf23-reduces-cyp27b1-expression Recombinant FGF23 lowers renal CYP27B1 mRNA before the fall in serum phosphate. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 restrains a vitamin D activation enzyme. organism: Mus musculus; Rattus norvegicus tissue_or_cell_type: Kidney experimental_model: Recombinant FGF23 injections in normal and parathyroidectomized rodents limitations: Injection study; transcript change is not direct enzyme inhibition. [shimada2004injection] FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis (2004). https://pubmed.ncbi.nlm.nih.gov/15040831/ DOI: 10.1359/JBMR.0301264
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Magnesium deprivation decreased renal cyp27b1-mrna abundance in the 21-day rat experiment.

    Magnesium → CYP27B1 mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Magnesium -> vitamin D/phosphate handling; transcript-level evidence.
    experimental_model
    Mg-free versus 0.05% Mg diet.
    limitations
    mRNA endpoint; no transporter flux or obligatory enzyme-bound Mg inference.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rattus norvegicus
    plain_language
    The kidney made less of the message for vitamin D activation.
    primary_references
    [mg-matsuzaki2013] Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats (2013). https://pubmed.ncbi.nlm.nih.gov/23816829/ DOI: 10.1684/mrh.2013.0341
    tissue_or_cell_type
    Rat kidney
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1382–1392

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mg-free versus 0.05% Mg diet. · source_derived_draft · unverified_draft

    ### mg-deficiency-cyp27b1-transcript Magnesium deprivation decreased renal cyp27b1-mrna abundance in the 21-day rat experiment. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney made less of the message for vitamin D activation. organism: Rattus norvegicus tissue_or_cell_type: Rat kidney experimental_model: Mg-free versus 0.05% Mg diet. limitations: mRNA endpoint; no transporter flux or obligatory enzyme-bound Mg inference. cross_nutrient: Magnesium -> vitamin D/phosphate handling; transcript-level evidence. [mg-matsuzaki2013] Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats (2013). https://pubmed.ncbi.nlm.nih.gov/23816829/ DOI: 10.1684/mrh.2013.0341
    Complete structured claim and evidence

  2. Magnesium depletion did not impair measured calcifediol-to-calcitriol conversion in these rats; isolated renal activity persisted without added Mg.

    Magnesium → Calcitriol production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Magnesium/vitamin D: qualify a universal CYP27B1 shutdown claim.
    experimental_model
    In-vivo tracer and isolated mitochondrial assays.
    limitations
    No-added-Mg buffer does not prove a metal-free preparation. This result cannot be generalized to every species or illness.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rattus norvegicus
    plain_language
    Low magnesium did not switch off vitamin D activation in this rat experiment.
    primary_references
    [mg-carpenter1987] Effect of magnesium depletion on metabolism of 25-hydroxyvitamin D in rats (1987). https://pubmed.ncbi.nlm.nih.gov/3605332/ DOI: 10.1152/ajpendo.1987.253.1.e106
    tissue_or_cell_type
    Rat circulation and isolated kidney mitochondria
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1370–1380

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In-vivo tracer and isolated mitochondrial assays. · source_derived_draft · unverified_draft

    ### mg-rat-calcitriol-conversion-preserved Magnesium depletion did not impair measured calcifediol-to-calcitriol conversion in these rats; isolated renal activity persisted without added Mg. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low magnesium did not switch off vitamin D activation in this rat experiment. organism: Rattus norvegicus tissue_or_cell_type: Rat circulation and isolated kidney mitochondria experimental_model: In-vivo tracer and isolated mitochondrial assays. limitations: No-added-Mg buffer does not prove a metal-free preparation. This result cannot be generalized to every species or illness. cross_nutrient: Magnesium/vitamin D: qualify a universal CYP27B1 shutdown claim. [mg-carpenter1987] Effect of magnesium depletion on metabolism of 25-hydroxyvitamin D in rats (1987). https://pubmed.ncbi.nlm.nih.gov/3605332/ DOI: 10.1152/ajpendo.1987.253.1.e106
    Complete structured claim and evidence

  3. All four homozygous CYP27B1 missense variants identified in four unrelated rickets patients abolished measured 1alpha-hydroxylase activity when expressed in COS-1 cells.

    Human CYP27B1 gene → Calcitriol production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Primary abstract, Methods and Results.
    experimental_model
    Patient sequencing and heterologous functional assays
    exposure
    Four patient-derived variants versus normal enzyme; dose/time not specified in abstract.
    limitations
    Functional loss is experimentally supported; clinical severity cannot be predicted solely from this assay.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens proteins in COS-1 cells
    plain_language
    An inherited enzyme defect can block the final activation step.
    primary_references
    [kitanaka1998] Inactivating mutations in the 25-hydroxyvitamin D3 1alpha-hydroxylase gene in patients with pseudovitamin D-deficiency rickets. (1998). https://pubmed.ncbi.nlm.nih.gov/9486994/ DOI: 10.1056/NEJM199803053381004
    tissue_or_cell_type
    renal activation machinery modeled in cultured cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 482–495

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient sequencing and heterologous functional assays · source_derived_draft · unverified_draft

    ### vd-act-cyp27b1-mutations All four homozygous CYP27B1 missense variants identified in four unrelated rickets patients abolished measured 1alpha-hydroxylase activity when expressed in COS-1 cells. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inherited enzyme defect can block the final activation step. organism: Homo sapiens proteins in COS-1 cells tissue_or_cell_type: renal activation machinery modeled in cultured cells experimental_model: Patient sequencing and heterologous functional assays limitations: Functional loss is experimentally supported; clinical severity cannot be predicted solely from this assay. exposure: Four patient-derived variants versus normal enzyme; dose/time not specified in abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and Results. nutrient: Vitamin D2 and D3 [kitanaka1998] Inactivating mutations in the 25-hydroxyvitamin D3 1alpha-hydroxylase gene in patients with pseudovitamin D-deficiency rickets. (1998). https://pubmed.ncbi.nlm.nih.gov/9486994/ DOI: 10.1056/NEJM199803053381004
    Complete structured claim and evidence

  4. The active human CYP27B1 reconstitution supplied human adrenodoxin reductase and NADPH upstream of human adrenodoxin.

    Human ferredoxin reductase / FDXR → Human adrenodoxin / FDX1 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Primary Tables 3-5, Figure 6A and Experimental procedures; full text retrieved.
    experimental_model
    Human protein reconstitution and substrate turnover
    exposure
    0.4 micromolar FDXR, 15 micromolar FDX1 and 50 micromolar NADPH; Experimental procedures.
    limitations
    This record reports the supported redox chain; FDXR omission or dietary niacin/riboflavin intervention was not reported in the extracted experiment.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens proteins
    plain_language
    A reductase feeds the electron carrier used during vitamin D activation.
    primary_references
    [tang2012] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles. (2012). https://pubmed.ncbi.nlm.nih.gov/22862690/ DOI: 10.1111/j.1742-4658.2012.08736.x
    tissue_or_cell_type
    mitochondrial redox-partner assay

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 467–480

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human protein reconstitution and substrate turnover · source_derived_draft · unverified_draft

    ### vd-act-fdxr-cyp27b1-system The active human CYP27B1 reconstitution supplied human adrenodoxin reductase and NADPH upstream of human adrenodoxin. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A reductase feeds the electron carrier used during vitamin D activation. organism: Homo sapiens proteins tissue_or_cell_type: mitochondrial redox-partner assay experimental_model: Human protein reconstitution and substrate turnover limitations: This record reports the supported redox chain; FDXR omission or dietary niacin/riboflavin intervention was not reported in the extracted experiment. exposure: 0.4 micromolar FDXR, 15 micromolar FDX1 and 50 micromolar NADPH; Experimental procedures. cross_nutrient: true evidence_location: Primary Tables 3-5, Figure 6A and Experimental procedures; full text retrieved. nutrient: Vitamin D2 and D3 [tang2012] Expression of human CYP27B1 in Escherichia coli and characterization in phospholipid vesicles. (2012). https://pubmed.ncbi.nlm.nih.gov/22862690/ DOI: 10.1111/j.1742-4658.2012.08736.x
    Complete structured claim and evidence

  5. Adding 100 nM 25(OH)D3 increased detectable 1, 25(OH)2D in conditioned monocyte medium even without TLR induction.

    Calcifediol / 25-hydroxyvitamin D3 → Calcitriol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human bone-clinic cohort and ex-vivo monocytes in 10% autologous serum
    exposure
    Human monocytes, 24 hours, 100 nMadded 25(OH)D3; Fig 3C.
    limitations
    Ex-vivo monocytes in 10% serum, not a whole-person infection endpoint. Low-substrate medium is not a validated universal blood threshold.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    These immune cells could activate the precursor locally.
    primary_references
    [adams2009] Vitamin d-directed rheostatic regulation of monocyte antibacterial responses. (2009). https://pubmed.ncbi.nlm.nih.gov/19299728/ DOI: 10.4049/jimmunol.0803736
    tissue_or_cell_type
    Human monocytes

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 996–1007

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human bone-clinic cohort and ex-vivo monocytes in 10% autologous serum · source_derived_draft · unverified_draft

    ### vd-adams-local-conversion Adding 100 nM 25(OH)D3 increased detectable 1, 25(OH)2D in conditioned monocyte medium even without TLR induction. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: These immune cells could activate the precursor locally. organism: Homo sapiens tissue_or_cell_type: Human monocytes experimental_model: Human bone-clinic cohort and ex-vivo monocytes in 10% autologous serum limitations: Ex-vivo monocytes in 10% serum, not a whole-person infection endpoint. Low-substrate medium is not a validated universal blood threshold. exposure: Human monocytes, 24 hours, 100 nMadded 25(OH)D3; Fig 3C. cross_nutrient: false [adams2009] Vitamin d-directed rheostatic regulation of monocyte antibacterial responses. (2009). https://pubmed.ncbi.nlm.nih.gov/19299728/ DOI: 10.4049/jimmunol.0803736
    Complete structured claim and evidence

  6. In monocytes cultured with 10% autologous serum, 19 kDa TLR2/1 agonist increased CYP27B1 yet reduced hCAP transcript; expression was enhanced by adding 5 nM 25(OH)D3.

    Mycobacterial 19 kDa lipopeptide TLR agonist → Human CAMP mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human bone-clinic cohort and ex-vivo monocytes in 10% autologous serum
    exposure
    24-hour ex-vivo culture; 10% autologous serum, with or without added 5 nM 25(OH)D3.
    limitations
    Ex-vivo monocytes in 10% serum, not a whole-person infection endpoint. Low-substrate medium is not a validated universal blood threshold.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    Making more activation machinery did not guarantee an antimicrobial response when substrate supply was limited.
    primary_references
    [adams2009] Vitamin d-directed rheostatic regulation of monocyte antibacterial responses. (2009). https://pubmed.ncbi.nlm.nih.gov/19299728/ DOI: 10.4049/jimmunol.0803736
    tissue_or_cell_type
    Human monocytes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 983–994

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human bone-clinic cohort and ex-vivo monocytes in 10% autologous serum · source_derived_draft · unverified_draft

    ### vd-adams-low-substrate In monocytes cultured with 10% autologous serum, 19 kDa TLR2/1 agonist increased CYP27B1 yet reduced hCAP transcript; expression was enhanced by adding 5 nM 25(OH)D3. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Making more activation machinery did not guarantee an antimicrobial response when substrate supply was limited. organism: Homo sapiens tissue_or_cell_type: Human monocytes experimental_model: Human bone-clinic cohort and ex-vivo monocytes in 10% autologous serum limitations: Ex-vivo monocytes in 10% serum, not a whole-person infection endpoint. Low-substrate medium is not a validated universal blood threshold. exposure: 24-hour ex-vivo culture; 10% autologous serum, with or without added 5 nM 25(OH)D3. cross_nutrient: false [adams2009] Vitamin d-directed rheostatic regulation of monocyte antibacterial responses. (2009). https://pubmed.ncbi.nlm.nih.gov/19299728/ DOI: 10.4049/jimmunol.0803736
    Complete structured claim and evidence

  7. Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced macrophage autophagy.

    Calcifediol / 25-hydroxyvitamin D3 → Macrophage autophagy source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human macrophage IFN-gamma experiments with sera of differing 25OHD content
    exposure
    IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.
    limitations
    Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    The cells recovered a recycling and defense process called autophagy.
    primary_references
    [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    tissue_or_cell_type
    Human macrophages
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1048–1059

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

    ### vd-fabri-autophagy Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced macrophage autophagy. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells recovered a recycling and defense process called autophagy. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    Complete structured claim and evidence

  8. Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced antimicrobial peptide expression.

    Calcifediol / 25-hydroxyvitamin D3 → Human CAMP mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human macrophage IFN-gamma experiments with sera of differing 25OHD content
    exposure
    IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.
    limitations
    Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    Adding precursor restored the antimicrobial gene response.
    primary_references
    [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    tissue_or_cell_type
    Human macrophages
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1035–1046

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

    ### vd-fabri-camp Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced antimicrobial peptide expression. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding precursor restored the antimicrobial gene response. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    Complete structured claim and evidence

  9. Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced phagosome-lysosome fusion.

    Calcifediol / 25-hydroxyvitamin D3 → Macrophage phagosome-lysosome fusion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human macrophage IFN-gamma experiments with sera of differing 25OHD content
    exposure
    IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.
    limitations
    Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    The compartment holding the pathogen could fuse with a degradative compartment.
    primary_references
    [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    tissue_or_cell_type
    Human macrophages
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1061–1072

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

    ### vd-fabri-fusion Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced phagosome-lysosome fusion. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The compartment holding the pathogen could fuse with a degradative compartment. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    Complete structured claim and evidence

  10. Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced antimicrobial activity against intracellularM. tuberculosis.

    Calcifediol / 25-hydroxyvitamin D3 → Intracellular Mycobacterium tuberculosis viability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human macrophage IFN-gamma experiments with sera of differing 25OHD content
    exposure
    IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.
    limitations
    Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    The cell experiment also recovered antimicrobial activity.
    primary_references
    [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    tissue_or_cell_type
    Human macrophages
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1074–1085

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

    ### vd-fabri-killing Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced antimicrobial activity against intracellularM. tuberculosis. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell experiment also recovered antimicrobial activity. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards