Prevention of murine experimental allergic encephalomyelitis: cooperative effects of cyclosporine and 1 α, 25-(OH)2D3

Brănișteanu, Dumitru; Waer, Mark; Sobis, H; Marcelis, Suzanne; Vandeputte, Michel; Bouillon, Roger

doi:10.1016/0165-5728(95)00076-e

Cited by 94 publications

(50 citation statements)

References 49 publications

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“…The active form of vitamin D is known as a powerful modulator of the immune system (27). The 1␣,25(OH) 2 D 3 -induced shift toward Th 2 differentiation can even prevent the onset of Th 1 -mediated autoimmune diseases, such as diabetes in NOD mice (28) or EAE in SJL/J mice (29).…”

Section: Discussionmentioning

confidence: 99%

Acute Shock Induced by Antigen Vaccination in NOD Mice

et al. 2003

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Type 1 diabetes in NOD mice can be prevented through autoantigen vaccination by shifting lymphocyte differentiation toward a T-helper 2 (Th 2 ) response. However, in other models of autoimmunity, this approach may be accompanied by unexpected triggering of Th 2 -dependent anaphylactic shock. To test the safety of vaccination therapy in the NOD mouse model, we evaluated the effects of immunization with a wide battery of antigens in NOD, BALB/c, and C57BL/6 mice. Surprisingly, a nondiabetogenic antigen, hen egg white lysozyme, induced severe shock exclusively in NOD mice (shock in 11 of 11 mice, lethal in 3 mice). Shock severity was further increased by a more pronounced Th 2 setting generated by 1␣,25(OH) 2 D 3 administration (17 of 17 mice, lethal in 14 mice, P < 0.0001). Pretreatment with dexamethasone resulted in full rescue, indicating an immune-mediated mechanism. Serum IgE levels and Th 1 /Th 2 cytokine profile analysis showed that the shock phenomenon was paralleled by a Th 2 response. mRNA expression of platelet-activating factor receptor (PAF-R) was significantly higher in NOD mice (P < 0.01) and was further increased by 1␣,25(OH) 2 D 3 . Pretreatment with WEB2086 (PAF-R antagonist) again protected all mice from lethal shock, indicating PAF as an anaphylaxis effector. In conclusion, in NOD mice, vaccination leading to a Th 2 immune shift can result in a lethal anaphylactic reaction. Diabetes 52:335-341, 2003

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Section: Discussionmentioning

confidence: 99%

Acute Shock Induced by Antigen Vaccination in NOD Mice

et al. 2003

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“…Vitamin D is also proved to be effective in the prevention and treatment of EAE [103][104][105][106][107] .…”

Section: Vitamin D and Msmentioning

confidence: 99%

Role of vitamin D in immune responses and autoimmune diseases, with emphasis on its role in multiple sclerosis

Zhang

2010

Neurosci. Bull.

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“…Withdrawal of 1,25-(OH) 2 D after EAE induction resulted in a resumption of clinical signs (Cantorna et al, 1996). The effect of 1,25-(OH) 2 D can be potentiated by cyclosporine, sirolimus (Rapamycin, RAP), and calcium (Branisteanu et al, 1995(Branisteanu et al, , 1997Cantorna et al, 1999). In EAE in mice, calcium was required in addition to 1,25-(OH) 2 D to prevent the appearance of this disease, and the higher the calcium intake the lower the 1,25-(OH) 2 D dose needed (Cantorna et al, 1999).…”

Section: Experimental Autoimmune Encephalomyelitis (Eae)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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Prevention of murine experimental allergic encephalomyelitis: cooperative effects of cyclosporine and 1 α, 25-(OH)2D3

Cited by 94 publications

References 49 publications

Acute Shock Induced by Antigen Vaccination in NOD Mice

Acute Shock Induced by Antigen Vaccination in NOD Mice

Role of vitamin D in immune responses and autoimmune diseases, with emphasis on its role in multiple sclerosis

Multiple sclerosis and vitamin D: an update

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