The effect of vitamin D supplementation on peripheral regulatory T cells and β cell function in healthy humans: a randomized controlled trial

Bock, Gerlies; Prietl, Barbara; Mader, Julia K.; Höller, Evelyne; Wolf, Michael; Pilz, Stefan; Graninger, Winfried; Obermayer–Pietsch, Barbara; Pieber, Thomas R.

doi:10.1002/dmrr.1276

Cited by 98 publications

(76 citation statements)

References 47 publications

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“…The vast majority of research in this area, however, has been in animal models or in vitro , and may or may not be reflective of the effects of vitamin D in vivo in humans. There have been a few randomized clinical trials where individuals were supplemented with vitamin D (in cholecalciferol form) and immunological changes studied; only one of these was in healthy individuals 103 , the remaining being in people with MS, 104–106 obesity, 107 or congestive heart failure. 108 These studies varied with respect to the dose and duration of vitamin D given and average levels of 25(OH)D achieved (Figure 4).…”

Section: Specific Risk Factorsmentioning

confidence: 99%

The initiation and prevention of multiple sclerosis

2012

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Although there are strong genetic determinants of multiple sclerosis, the results of migration studies support a role for the environment, and through rigorous epidemiological investigation, Epstein-Barr virus infection, vitamin D nutrition, and cigarette smoking have been identified as likely causal factors for multiple sclerosis. In this review, we discuss the strength of this evidence, as well as the potential biological mechanisms underlying these associations. Both vitamin D nutrition and cigarette smoking are modifiable and as such, increasing vitamin D levels and smoking avoidance have the potential to substantially reduce MS risk and influence its progression.

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Section: Specific Risk Factorsmentioning

confidence: 99%

The initiation and prevention of multiple sclerosis

2012

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“…Following a period of 6-8 month of breast-feeding, infants were randomized into either receiving hydrolyzed casein-based or conventional cow's milk formula 12 . The randomization code will be opened when the last recruited child turns 10 years of age, which is not until 2017 (ref 13) It has been speculated that vitamin D protects against islet autoimmunity, T1D, or both 15 possibly through effects on T lymphocytes 16 . Lower concentrations of vitamin D have been reported in T1D children and lower vitamin D levels during pregnancy were suggested to increase the risk for T1D 17 .…”

Section: Primary Prevention -Treating Subjects At Genetic Risk For Ismentioning

confidence: 99%

“…Alum-formulated recombinant human GAD65 tested in Phase II and III clinical trials were found to be safe [38][39][40] . The immunomodulating effect seemed to include the induction of Treg cells 16,38 and the residual beta-cell function in newly diagnosed T1D patients. We have randomized a total of 50 children in the trial Diabetes Prevention -Immune Tolerance (DIAPREV-IT) to either placebo or alum-formulated GAD65 in a prime and boost design (NCT01122446).…”

Section: Glutamic Acid Decarboxylase (Gad65)mentioning

confidence: 99%

Immune therapy in type 1 diabetes mellitus

Lernmark

Larsson

2013

Nat Rev Endocrinol

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(200 words) Type 1 diabetes mellitus (T1D) is an autoimmune disorder directed against the pancreatic islet β cells. The genetic risk for the disease is linked to HLA-DQ genotypes and unknown environmental triggers. In most countries, only 10-15% of newly diagnosed T1D children or young adults have a first degree relative with the disease. Autoantibodies against insulin, GAD65, IA-2 or ZnT8 transporter mark islet autoimmunity. These islet autoantibodies may develop already at 1-2 years of age. Immune therapy in T1D is approached at three stages. Primary prevention is treatment of subjects at increased genetic risk. The TRIGR trial is testing if hydrolyzed casein milk formula may reduce T1D in genetically predisposed infants. Secondary prevention is in subjects with persistent islet autoantibodies. On-going trials are either non-autoantigen (BCG, CD3 monoclonal antibodies) or autoantigen (oral and nasal insulin or Alum-formulated GAD65) specific. Intervention at diabetes onset include non-autoantigen (CD3 monoclonal antibodies, IL-2 receptor antibodies, Il-1b receptor inhibitor, Il-1b antibodies, BCG, ATG, DiaPep277) and autoantigen (proinsulin peptides) specific therapy. Although preserved beta-cell function long term has been difficult to achieve in many prior studies, considerable progress is being made through controlled clinical trials and animal investigations to uncover mechanisms of beta-cell destruction. Novel therapies that would prevent islet autoimmunity or halt progressive beta-cell destruction need to be designed.

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“…Here an improvement in β-cell function could not be confirmed but subjects featured an increase in Treg frequency in the peripheral blood. 15 In view of the clinical application of vitamin D, a balance between an optimal dose and calcaemic side effects needs to be investigated. Current research is focusing on vitamin D analogs that dissociate between an optimal immunomodulatory dose range and toxic calcaemic effects.…”

Section: Ctla4-immunoglobulin Fusion Protein (Abatacept)mentioning

confidence: 99%