Vitamin D receptor gene polymorphism in Egyptian multiple sclerosis patients.

One of the most common neurological illnesses in the world is multiple sclerosis (MS), a chronic autoimmune demyelinating disease of the central nervous system (CNS). MS has both a genetic and an environmental origin. In terms of environmental factors, vitamin D deficiency is one of the most important risk factors and closely connected with gene polymorphisms involved in vitamin D metabolism, transport, or activity. Since vitamin D activity requires a receptor-mediated response, any changes to the vitamin D receptor (VDR) may have an effect on the pathophysiology of the disease. In this study, we aimed to identify the relationship between VDR gene polymorphisms, FokI A>G (rs2228570), ApaI A>C (rs7975232) and BsmI C>T (rs1544410) and MS. FokI, ApaI and BsmI genotypes were determined in 50 patients with relapsing remitting MS (RRMS) and in 50 control subjects. DNA was isolated from blood samples, and then FokI, ApaI and BsmI gene polymorphisms were identified using allelic discrimination real time polymerase chain reaction (PCR) assay. The distribution of FokI, ApaI and BsmI polymorphisms did not show any significant differences between MS patients and controls. Thus, we concluded that there is no association between the studied VDR gene polymorphisms and MS.

Vitamin D Increases Percentages of Interleukin-10 Secreting Regulatory T Cells in Children with Cow's Milk Allergy.

Cow's milk allergy (CMA) is known to be either IgE- or non-IgE mediated. Regulatory T (Treg) cell defect is involved in the pathogenesis of both types. Vitamin D has been suggested to improve the generation of allergen-specific Treg cell populations with the potential to provide safe and long-term alleviation of disease symptoms. This study aimed to assess Vitamin D status in children with physician-diagnosed CMA and to investigate the effect of in vitro cultivation with Vitamin D on the percentage of antigen-driven CD4+CD25highFoxp3+IL10+ Treg cells following in vitro stimulation of cells with cow's milk allergen in culture. This cross-sectional study included 20 children with CMA and 20 healthy age and sex-matched children as a control group. All patients were subjected to clinical evaluation, cow's milk skin prick test (SPT), cow's milk elimination and oral re-challenge test in patients with negative cow's milk SPT and in those with gastrointestinal presentation, measurement of serum Vitamin D level and assessment of the percentage of antigen-driven CD4+CD25highFoxp3+IL10+ Treg cells in response to stimulation with cow's milk allergen extract with and without Vitamin D in culture. Vitamin D deficiency was detected in 80% of children with CMA. Percentage of Foxp3+ and IL10+ co-expression on Treg cells was significantly increased after stimulation with cow's milk allergen extract in the presence of Vitamin D. A significant positive correlation was observed between serum Vitamin D level and percentage of antigen-driven CD4+CD25highFoxp3+IL10+ Treg cells as well as level of Foxp3+ and IL10+ co-expression on Treg cells at baseline (control cultures without stimulation) and after PBMCs stimulation with cow's milk allergen extract in the presence of Vitamin D. Re-stimulation with cow's milk allergen extract was performed in vitro in order to evaluate milk-induced immune stimulation and regulation. In conclusion, patients with CMA whether IgE- or non-IgE mediated had Vitamin D deficiency with a decreased number of CD4+CD25highFoxp3+IL10+ Treg cells which increased after in vitro addition of Vitamin D with increased Foxp3 and IL10 co-expression.