Vitamin D and the Immune System

Vitamin D receptors (VDR) are expressed on nearly every immune cell type — including T cells, B cells, dendritic cells, macrophages, and neutrophils. The active metabolite 1,25-dihydroxyvitamin D acts as an immunomodulator, tuning both the innate response to pathogens and the tolerance mechanisms that limit autoimmunity.

Innate immunity: cathelicidin and defensins

When toll-like receptor 2 on macrophages recognises a pathogen (e.g., Mycobacterium tuberculosis), it upregulates CYP27B1 and VDR. Local 25(OH)D is converted to the active 1,25-dihydroxyvitamin D, which then drives transcription of cathelicidin (LL-37) and β-defensin-2 — antimicrobial peptides that puncture pathogen membranes. Individuals with low 25(OH)D produce less cathelicidin per macrophage stimulation (Liu et al. 2006).

Adaptive immunity: T-cell modulation

1,25-dihydroxyvitamin D biases the T-helper response away from pro-inflammatory Th1/Th17 profiles toward Th2 and regulatory T cells (Treg). It also inhibits dendritic-cell maturation, reducing antigen presentation. The net effect is dampened autoimmunity — a mechanism consistent with epidemiological links between low vitamin D and multiple sclerosis, type 1 diabetes, and inflammatory bowel disease.

What the randomised trials show

Practical implications

The consistent message is that correcting deficiency yields the clearest immunological benefit. Supplementing a person who is already sufficient (≥ 30 ng/mL) is unlikely to further improve infection resistance. If you or your children get frequent respiratory infections and haven't measured your 25(OH)D, it's a reasonable test to request.

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