The response to HBV vaccine in celiac children who were compliant to GFD is not different from a healthy population. CD may be one of the immune diseases associated with a high rate of HBV vaccine nonresponse but it might not be permanent and treatment with GFD and compliance to the treatment may ameliorate the immune response to HBV vaccine in celiac children.
To determine the optimal time of Bacillus Calmette-Guerin (BCG) vaccination for induction of Th1 immunity, we measured the interferon (IFN)-γ and interleukin (IL)-10 secretion in purified protein derivative (PPD)-stimulated peripheral blood mononuclear cell (PBMC) cultures in newborns vaccinated at birth or 2nd month of life. Moreover, role of CD4(+) CD25(+) T cells was studied by depletion assay at 8th month. Nineteen term and healthy newborns were randomized into two groups: Group I composed of 10 newborns vaccinated with BCG at birth and the remaining 9 (group II) at 2nd month of life. PBMCs were isolated at birth, 2nd and 8th months of age, and PPD-stimulated IL-10, 5 and IFN-γ secretion were assessed. The same measurements were repeated for IL-10 and IFN-γ after the depletion of CD4(+) CD25(+) T cells at the 8th month. Children vaccinated at birth demonstrated higher PPD-stimulated IFN-γ and IL-10 levels at 2 months of age when compared to non-vaccinated ones (p = 0.038 and p = 0.022, respectively), whereas at 8 months, no significant differences were detected between the two groups. Moreover, CD4(+) CD25(+)-depleted T-cell cultures resulted in lower PPD-stimulated IL-10 levels in those vaccinated at birth when compared to non-depleted condition at the 8th month (p < 0.001). BCG at birth upregulated PPD-stimulated IFN-γ secretion at the 2nd month and remained still detectable at 8 month after the vaccination, whereas those vaccinated at the 2nd month of life lacked that increase in IFN-γ response at the same time-point. Furthermore, depletion assays suggest that CD4(+) CD25(+) T cells are involved in PPD-stimulated IL-10 secretion in response to BCG vaccination.
Background and Aim: Vitamin D receptor (VDR) gene polymorphisms have been implicated in the pathogenesis of many diseases, such as periodontitis and diabetes mellitus (DM). The present study aimed to evaluate the distributions of VDR polymorphisms in diabetic individuals with healthy periodontium (DMH), diabetic individuals with periodontitis (DMP), nondiabetic individuals with healthy periodontium (H), and nondiabetic individuals with periodontitis (P). Material and Methods: A total of 200 individuals (DMH = 40, DMP = 60, H = 40, and P = 60) were recruited. All clinical periodontal parameters, demographical, and biochemical variables were recorded. Blood samples were collected, and genomic DNA was isolated by Purelink® Genomic DNA Mini Kit. Genotyping of VDR polymorphisms ApaI, BsmI, FokI, and TaqI were determined by real-time polymerase chain reaction (PCR) using allele-specific probes. Results: The distribution of the BsmI variant showed differences between DMH and H groups (P = 0.034). In addition, carrying the GG genotype (OR = 0.317; 95% CI = 0.126–0.797; P = 0.013) and the G allele (OR = 2.373; 95% CI = 1.203–4.681; P = 0.012) increased the risk of type 2 DM. Moreover, it was determined that the frequency of CC genotype of FokI variant was higher in DMP compared to DMH (P = 0.046). It was determined that having the CC genotype (OR = 2.706; 95% CI = 1.185–6.176; P = 0.017) and the C allele (OR = 1.917; 95% CI = 0.995–3.694; P = 0.049) increased the risk of periodontitis among diabetic individuals. No differences were detected among groups in the genotype and allele distributions of ApaI and TaqI variants (P > 0.05). Conclusions: The present study showed that the BsmI variant was a risk factor for DM among periodontally healthy individuals and the FokI variant for periodontitis among diabetic individuals.
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