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The prevalence of vitamin D deficiency has been shown to be increased in many of the common arthritides. Importantly, vitamin D has significant immunomodulatory effects in addition to its role in calcium homoeostasis. Both aspects of its function have a major bearing on joint disease whether as part of an inflammatory arthritis or from wear and tear. While the exact mechanisms still require clarification, there is now compelling evidence that the hormonally active 1,25-dihydroxycholecalciferol vitamin D can reduce the activity of the proinflammatory Th1 and Th17 T cell subsets. Additionally, it is stimulatory of enhanced anti-inflammatory Th2 activity at the same time as promoting T regulatory cell activity. These various actions suggest that correcting vitamin D deficiency should be a important part of the management of all patients with joint disease. For the future, vitamin D analogues with enhanced immunomodulatory properties but with reduced ability to increase calcium are being investigated.
Department of Immunology, Epsom and St Helier University Hospitals NHS Trust, Carshalton, Surrey, SM5 1AA, UK, Amolak.Bansal@ESTH.nhs.uk.
This article was published in the following journal.
Name: Rheumatology international
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A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
Alteration of the immune system or of an immune response by agents that activate or suppress its function. This can include IMMUNIZATION or administration of immunomodulatory drugs. Immunomodulation can also encompass non-therapeutic alteration of the immune system effected by endogenous or exogenous substances.
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