The adaptive immune response in Graves’ Disease: Does Vitamin D have a role? / Journal of the ASEAN Federation of Endocrine Societies

@#Graves' disease (GD) is an autoimmune disease characterized by excessive autoantibody formation by the lymphocyte B cells (B cells). The autoantibodies will bind to Thyroid Stimulating Hormone receptors (TSHR) and enhance the production of thyroid hormone. Previous studies indicate that the impairment of immune response in GD happens in several points in the adaptive immune response, particularly the profile of the intrathyroidal dendritic cells (tDC), the imbalance of T helper-1 (Th1) and T helper-2 (Th2), the Th17 cells that act as pro-inflammatory cells and the dysfunction of immune modulating T regulator (Treg) cells.6-11 Vitamin D is a steroid hormone which has pleiotropic effects. The role of vitamin D in bone and calcium metabolism is already established. The discovery of vitamin D receptor (VDR) in immune cells such as monocytes/macrophages, T cells and B cells, demonstrates that vitamin D may influence innate and adaptive immune process. Recent studies try to explore the relationship between vitamin D and autoimmune disease, furthermore they consider vitamin D as a modifiable environmental factor in autoimmune diseases.13,40 Most people with autoimmune diseases have lower vitamin D level than that of healthy subjects. Vitamin D level also has been associated with disease activity of Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). Vitamin D influences adaptive immune response through its ability to modulate dendritic Cells (DC), T cells, B cells and Treg cells. Although previous studies reported the immune response disturbance in GD include the tDC, Thelper and Treg cells,6-11 little is known whether the immunoregulatory effect of vitamin D can interfere with the natural history of GD. The effect of vitamin D in GD remains to be explored.

The role of allergic risk and other factors that affect the occurrence of atopic dermatitis in the first 6 months of life

BACKGROUND: Atopic dermatitis (AD) is a chronic inflammation of the skin that often appears in early childhood. The manifestation is related to the tendency towards T helper 2 cytokine immune responses (interleukin (IL)-4, IL-5). Genetic factors are suggested to play important roles in AD, and it can be transmitted to newborns, increasing their risk of developing allergies. OBJECTIVE: To determine the association between cord-blood cytokine levels (IL-5, interferon (IFN) γ), cord-blood total immunoglobulin E (IgE) level, perinatal environmental exposure, and the risks of allergy as well as the development of AD in the first 6 months of life. METHODS: A 6-month cohort study with a nested case-control within was conducted on newborns in Jakarta from December 2008 until May 2009. After the umbilical cord blood samples were taken and stored, subjects were followed up monthly until 6 months old. The occurrence of AD and lifestyle or environmental exposures were recorded. The allergic risk was determined using a modified pediatric allergy immunology work groups scoring system based on allergic history (allergic rhinitis, asthma, AD) in the family. The levels of IL-5 and IFN-γ were measured using ELISA and total IgE by CAP system FEIA. Multivariate analysis was used to evaluate risk factors. RESULTS: This study was conducted on 226 subjects. The incidence of AD was 16.4%; of those, 59% had low risk allergy, 38.5% moderate, and 2% high risk. AD mostly occurred at the age of 1 month (57%). Cord blood samples were examined in 37 subjects with AD and 51 without AD; of those, 25% showed high levels of total IgE (>1.2 IU/µL), and 51% showed normally-distributed high absorbance IL-5 values (≥0.0715, absolute value was undetected). The increased level of IL-5 was directly proportional to IgE. High absorbance IFN-γ values (≥0.0795, absolute value = 18.681 pg/µL) were observed in 52% of subjects. CONCLUSION: The associations between the risk of allergy in the family, cord-blood total IgE, IL-5, IFN levels, and some perinatal environmental exposure with AD in the first 6 months of life have not been established.