This 2019 Finnish review focused on vitamin D’s immune system effects:
“The epigenome of human monocytes is at multiple levels sensitive to vitamin D. These data served as the basis for the chromatin model of vitamin D signaling, which mechanistically explains the activation of a few hundred primary vitamin D target genes.
Vitamin D and its receptor are able to antagonize the pro-inflammatory actions of the transcription factors nuclear factor activated T cells (NF-AT) and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) in T cells. In this way, vitamin D reduces autoimmunity, such as the onset and progression of multiple sclerosis, as well as chronic inflammation.
Population-wide recommendations do not take inter-individual variations into account, such as a different molecular response to vitamin D, which are expressed by the vitamin D response index. Instead of population-based recommendations for vitamin D3 supplementation there should be personalized recommendations in order to reach a vitamin D status that is optimized for an individual’s health protection.
Trained immunity implies that immune cells memorize challenges, to which they are exposed in their rather short lifespan, in form of changes of their epigenome leading to subtype specification. The stabilization of the epigenomes of the subtypes of monocytes, macrophages and dendritic cells by vitamin D can prevent or delay the onset of common age-related diseases.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6753645/ “Vitamin D Signaling in the Context of Innate Immunity: Focus on Human Monocytes”
One of the five elements of the clinical trial Reversal of aging and immunosenescent trends was daily 3,000 IU vitamin D3 supplementation for nine months. That study’s monocyte findings included:
“Analysis of CyTOF‐defined immune cell populations revealed the most robust changes to be decreases in total and CD38‐positive monocytes and resulting increases in the lymphocyte‐to‐monocyte ratio (LMR). The changes in mean monocyte populations persisted 6 months after discontinuation of treatment, and the increase in LMR remained highly significant at 18 months as well.”