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Purpose: The aim of this study was to conduct a meta-analysis for single nucleotide polymorphisms (SNPs) in interleukin-13 (IL-13) and cluster of differentiation 14 (CD14) genes and the risk for allergic rhinitis (AR).Methods: We screened studies identified through seven databases including Pubmed, Medline, Web of Science, Embase, China Biology Medicine disc, Wanfang, and China Academic Journal Network Publishing Database. The odds ratios (ORs) and 95% confidence intervals (CIs) were determined to assess the association under allelic, dominant and recessive models.Results: Twelve studies with a total of 8547 participants (3223 cases and 5324 controls) investigated IL-13 SNP rs20541, five studies combining 4580 participants (1411 cases and 3169 controls) examined IL-13 SNP rs1800925, and nine studies with 2301 participants (1174 cases and 1127 controls) assessed CD14 SNP rs2569190. We found that the A allele of IL-13 SNP rs20541 was associated with an increased risk of AR (OR 1.19, 95% CI 1.11-1.28, P < 0.001). Stratifying studies by ethnic group produced significant results in Asians (OR 1.21, 95% CI 1.11-1.32, P < 0.001), but not in Caucasians (OR 1.14, 95% CI 1.00-1.30, P = 0.051). No association of IL-13 SNP rs1800925 and CD14 SNP rs2569190 with AR risk was found in either Asians or Caucasians (P > 0.05).Conclusion: Our findings suggest that IL-13 SNP rs20541 is significantly associated with AR risk in Asians but not in Caucasians. However, the accumulating evidence does not support an association of IL-13 SNP rs1800925 and CD14 SNP rs2569190 with AR risk. [ABSTRACT FROM AUTHOR]

Background: Previous studies have provided conflicting evidence implicating the IL-13 C-1112T and G2044A polymorphisms in Graves' disease (GD) risk. We undertook a meta-analysis to address this issue. Methods: The Medline, Pubmed and Web of Science databases were searched for published case-control studies investigating the relation of the IL-13 C-1112T and G2044A polymorphisms with GD risk. Data were extracted using standardized forms and odds ratios (OR) with 95% confidence intervals (CI) were calculated. Results: Available data did not suggest an association between any of the two IL-13 polymorphisms and GD risk. For the C-1112T polymorphism, the combined OR was 0.96 (95% CI: 0.77-1.19) for dominant model (TT + CT vs CC), 0.97 (95% CI: 0.69-1.38) for recessive model (TT vs CT + CC), and 0.97 (95% CI: 0.68-1.39) for homozygote model (TT vs CC). ORs for the G2044A polymorphism were similar. In subgroup analyses stratified by ethnicity, we also did not find associations between these two variants and GD risk in Asians or Caucasians. Sensitivity analyses by excluding each of the involved study in turn did not change the pooled results. Conclusion: The IL-13 C-1112T and G2044A polymorphisms are not associated with GD risk. [ABSTRACT FROM AUTHOR]

Background: Data on the association between the interleukin-1 (IL-1) gene polymorphisms and Graves' disease (GD) risk were conflicting. A meta-analysis was undertaken to assess this association. Methods: We searched for case-control studies investigating the association between the IL1B (-511), IL1B (+3954), IL1RN (VNTR) polymorphisms and GD risk. We extracted data using standardized forms and calculated odds ratios (OR) with 95% confidence intervals (CI). Results: A total of 11 case-control studies were included in this meta-analysis. Available data indicated that the IL1B (-511) polymorphism was associated with GD risk in the overall populations (Caucasians and Asians) in homozygote model (TT vs. CC, OR = 0.86, 95% CI: 0.76–0.97, Pz = 0.015), but not in dominant and recessive models (TT+TC vs. CC: OR = 0.95, 95% CI: 0.81–1.12, Pz = 0.553 and TT vs. TC+CC: OR = 0.82, 95% CI: 0.60–1.12, Pz = 0.205, respectively). No association between the IL1B (+3954), IL1RN (VNTR) polymorphisms and GD risk was found in the overall populations in any of the genetic models. In subgroup analyses according to ethnicity, the IL1B (-511) polymorphism was associated with GD risk in Asians in recessive and homozygote models (TT vs. TC+CC: OR = 0.68, 95% CI: 0.55–0.84, Pz<0.001 and TT vs. CC: OR = 0.81, 95% CI: 0.70–0.93, Pz = 0.003, respectively), but not in dominant model (TT+TC vs. CC: OR = 0.92, 95% CI: 0.77–1.11, Pz = 0.389). No association between the IL1B (+3954), IL1RN (VNTR) polymorphisms and GD risk was indicated in Asians, and we found no association between the IL1B (-511), IL1B (+3954), IL1RN (VNTR) polymorphisms and GD risk in Caucasians in any of the genetic models. Conclusion: The IL1B (-511) polymorphism, but not the IL1B (+3954) and IL1RN (VNTR) polymorphisms was associated with GD risk in Asians. There was no association between these polymorphisms and GD risk in Caucasians. [ABSTRACT FROM AUTHOR]

The aim of this study was to analyze whether regulatory CD4+CD25+ T lymphocytes exist and function normally in patients with atopic asthma. Our data showed that a significant increase in CD4+CD25+ cell numbers was seen in atopic asthmatics during acute exacerbation, but not in those stable asthmatics, atopic nonasthmatics, and normal subjects. The mean inhibition values of the proliferation response of CD4+CD25− cells by CD4+CD25+ cells from normal controls and asthmatics were almost the same. There was no difference in inhibitory effects on both Th1 and Th2 cytokine production of CD4+CD25− cells by CD4+CD25+ cells in the two groups. These data demonstrated that although CD4+CD25+ cells increase in atopic asthma during exacerbation, these regulatory T cells appear to function normally with regard to suppression of T-cell proliferation as well as Th1–Th2 cytokine production. [Copyright &y& Elsevier]

Objective: Single-stranded DNA-binding protein 1 (SSBP1) plays an important role in DNA repair processes and the maintenance of genomic stability. The aim of this study was to evaluate the expression of SSBP1 and its prognostic value in lung adenocarcinoma (LUAD) using bioinformatics approaches., Methods: We applied databases including UALCAN, Kaplan-Meier plotter, LinkedOmics, Webgestalt, cBioPortal and TIMER2.0 in this study., Results: We found that SSBP1 expression was up-regulated in LUAD samples and was correlated with clinicopathological features including age, cancer stage, and nodal metastasis status by the UALCAN analysis. Multivariate Cox regression analysis by the Kaplan-Meier plotter showed that high SSBP1 expression was independently correlated with poor overall survival (hazard ratio = 1.63, 95% confidence interval: 1.08-2.46, logrank P = 0.02). The LinkedOmics analysis showed that 5078 genes were positively correlated with SSBP1 expression, whereas 7905 genes were negatively correlated with SSBP1 in LUAD. Functional enrichment analysis using the Webgestalt tool showed that for SSBP1 and the genes positively correlating with it, the significantly enriched biological process was ribosomal large subunit biogenesis, and the significantly enriched pathway was proteasome. According to the cBioPortal database, the frequency of SSBP1 alterations was 1.7% in LUAD patients, and patients with SSBP1 alterations had worse prognosis (logrank P = 4.26e-05) compared with those unaltered for SSBP1. Finally, SSBP1 expression was negatively correlated with B cell infiltration level (Rho = -0.193, P = 1.54e-05) and the expression of B cell biomarkers including CD79A and CD19., Conclusion: Our results suggest that SSBP1 may be a prognostic marker for human LUAD.

Background: There is no consensus regarding the association between polymorphisms in the myosin IXB (MYO9B) gene and celiac disease (CD) risk. In this study, we performed a meta-analysis to evaluate genetic variants in MYO9B with CD., Methods: Four MYO9B polymorphisms (rs1545620, rs1457092, rs2305767 and rs2305764) were assessed. A literature search was conducted using PubMed, Scopus, and Web of Science databases until June 2015. Odds ratio (OR) and 95% confidence interval (CI) were used to investigate the strength of the association under dominant, recessive, homozygote and allelic comparison models., Results: Seven case-control studies with a total of 1965 CD patients and 4894 controls were included in this meta-analysis. The results showed that rs1545620 was associated with CD risk in Europeans in dominant (OR=1.31, 95% CI: 1.10-1.58, Pz =0.003), recessive (OR=1.36, 95% CI: 1.08-1.72, Pz =0.009), homozygote (OR=1.55, 95% CI: 1.20-2.01, Pz =0.001), and allelic comparison models (OR=1.24, 95% CI: 1.10-1.40, Pz =0.001), whereas in a Latin American group there were significant associations of CD with rs1457092 in dominant (OR=15.30, 95% CI: 3.51-66.67, Pz <0.001), homozygote (OR=16.55, 95% CI: 3.62-75.65, Pz <0.001), and allelic comparison models (OR=1.95, 95% CI: 1.31-2.91, Pz =0.001), and rs2305767 in dominant (OR=5.35, 95% CI: 2.42-11.86, Pz <0.001) and allelic comparison models (OR=1.65, 95% CI: 1.11-2.45, Pz =0.013). There was no association between rs2305764 and CD risk in either Europeans or the Latin American group., Conclusion: rs1545620 is associated with CD risk in Europeans, whereas rs1457092 and rs2305767 are associated with CD risk in a Latin American group.

Background: Antigen-loaded eosinophils (EOSs) instilled intratracheally into mice were capable of inducing Th2-type cytokine production in the draining lymph nodes. The aim of the present study was to evaluate whether EOSs within the tracheobronchial lumen can stimulate Th2 cell expansion in the lung tissues., Methods: Airway EOSs were recovered from ovalbumin-sensitized and -challenged BALB/c mice, these EOSs were then cocultured with CD4+ cells isolated from sensitized mice in the absence or presence of anti-CD80 or/and -CD86 monoclonal antibodies. Airway EOSs were instilled into the trachea of sensitized mice. At the day 3 thereafter, the lung tissues were removed and prepared into cell suspensions for culture. Cell-free culture supernatants were collected for detection of cytokines., Results: Airway EOSs functioned as CD80- and CD86-dependent antigen-presenting cells to stimulate lung CD4+ lymphocytes to produce interleukin-4, interleukin-5 and interleukin-13, but not interferon-gamma in in vitro assay. When instilled intratracheally in sensitized recipient mice, airway EOSs primed lung Th2 cells in vivo for interleukin-4, interleukin-5 and interleukin-13, but not interferon-gamma, production during the in vitro culture that was also CD80- and CD86-dependent., Conclusion: EOSs within the lumina of airways could process inhaled antigen and function in vitro and in vivo as antigen-presenting cells to promote expansion of Th2 cells in the lungs.