Interactions of 1,25-dihydroxyvitamin D3 and the immune system

Manolagas, Stavros C.; Provvedini, D; Tsoukas, Constantine D.

doi:10.1016/0303-7207(85)90074-7

Cited by 179 publications

(82 citation statements)

References 41 publications

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“…1,25-(OH) 2 D decreases the production of proinflammatory cytokines IL-2, IFN-g and TNF-a in vitro and in vivo (Manolagas et al, 1985;Reichel et al, 1989;Lemire & Adams, 1992), and IL-12 in vivo (Lemire et al, 1994;D'Ambrosio et al, 1998;Mattner et al, 2000). On the other hand, it promotes the in vivo production of anti-inflammatory cytokines such as IL-4 and TGF-b (Cantorna et al, 1998).…”

Section: Cytokines and Nitric Oxide (No)mentioning

confidence: 99%

Multiple sclerosis and vitamin D: an update

et al. 2004

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MS is a chronic, immune-mediated inflammatory and neurodegenerative disease of the central nervous system (CNS), with an etiology that is not yet fully understood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest. It is well recognized that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH) 2 D), is a natural immunoregulator with anti-inflammatory action. The mechanism by which vitamin D nutrition is thought to influence MS involves paracrine or autocrine metabolism of 25OHD by cells expressing the enzyme 1a-OHase in peripheral tissues involved in immune and neural function. Administration of the active metabolite 1,25-(OH) 2 D in mice and rats with experimental allergic encephalomyelitis (EAE, an animal model of MS) not only prevented, but also reduced disease activity. 1,25-(OH) 2 D alters dendritic cell and T-cell function and regulates macrophages in EAE. Interestingly, 1,25-(OH) 2 D is thought to be operating on CNS constituent cells as well. Vitamin D deficiency is caused by insufficient sunlight exposure or low dietary vitamin D 3 intake. Subtle defects in vitamin D metabolism, including genetic polymorphisms related to vitamin D, might possibly be involved as well. Optimal 25OHD serum concentrations, throughout the year, may be beneficial for patients with MS, both to obtain immune-mediated suppression of disease activity, and also to decrease disease-related complications, including increased bone resorption, fractures, and muscle weakness.

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Section: Cytokines and Nitric Oxide (No)mentioning

confidence: 99%

Multiple sclerosis and vitamin D: an update

et al. 2004

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“…Vitamin D is also involved in interleukin-2 (IL-2) inhibition and antibody production and in lymphocyte proliferation suppression and the generation of cytotoxic lymphocytes. 6,7 In addition, monocytes constitutively express VDR, as well as activated but not resting lymphocytes. 8,9 Within the rheumatoid joint, the active form of vitamin D has been shown to be synthesized in RA synovium and is thought to be stimulated by interleukin-1 (IL-1) and/or IL-2.…”

Section: Introductionmentioning

confidence: 99%

Association study of VDR gene with rheumatoid arthritis in the French population

et al. 2005

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“…The active vitamin D metabolite, 1,25-dihydroxyvitamin D3 (1 ,25-[OH]2-D3),' has been shown to exert immunosuppressive properties in vitro (1,2). We (3,4) and others (5)(6)(7) have previously demonstrated a significant inhibition of DNA synthesis, immunoglobulin, and IL-2 production by activated peripheral blood mononuclear cells in the presence of increasing concentrations of the active metabolite.…”

Section: Introductionmentioning

confidence: 99%