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Background:Nonalcoholic fatty liver disease (NAFLD) is emerging as a public health issue worldwide and is highly prevalent in patients with type 2 diabetes mellitus (T2DM). However, there was a great disparity across studies in the estimated prevalence of NAFLD in T2DM patients. This meta-analysis, therefore, aimed to estimate the pooled prevalence of NAFLD in T2DM patients.Methods:Electronic databases of PubMed, Web of Science, Embase, Chinese National Knowledge Infrastructure, and Wanfang were searched using MeSH terms to identify relevant studies. Eligibility assessment and data extraction were conducted independently by 2 investigators and a meta-analysis was performed to synthesize the data. Heterogeneity was evaluated using the Cochran Q test and quantified using the I2 statistic. Publication bias was assessed using both the Begg and Egger tests. Subgroup analyses were performed to identify the possible sources of heterogeneity.Results:Twenty-four studies involving 35,599 T2DM patients were included in this meta-analysis, of which 20,264 were identified with NAFLD. A high degree of heterogeneity (I2 = 99.0%, P < .001) was observed among the eligible studies, with the reported prevalence ranging from 29.6% to 87.1%. The pooled prevalence of NAFLD in T2DM patients, by a random-effects model, was 59.67% (95% confidence interval: 54.31–64.92%). Sensitivity was low and both the Begg test and Egger test showed low possibility of publication bias. Subgroup analyses indicated that the prevalence of NAFLD in T2DM patients differed by gender, obesity, hypertension, dyslipidemia, coronary heart disease, and chronic kidney disease.Conclusions:The high pooled prevalence of NAFLD in T2DM patients found in this study significantly underscores the need for early assessment of NAFLD and the importance of strengthening the management of NAFLD in T2DM patients.

Plasmacytoid dendritic cells (pDC) are rare cells found in peripheral blood and lymphoid tissues. pDC are considered to be “professional” type I interferon (IFN) producing cells and produce 10–100-fold more IFN-α than other cell types in response to enveloped viruses or synthetic TLR-7 and -9 agonists. In this study, purified pDC were found to express high levels of IFN-λ receptor mRNA as well as cell-surface IFN-λ receptor. We have developed intracellular flow cytometry assays using antibodies to IFN-λ1/3 or -λ2 to assess the expression of IFN-λ proteins by pDC. We observed that a subset of human pDC expresses only intracellular IFN-α while another subset produces both IFN-α and IFN-λ after stimulation with virus or the TLR9 agonist, CpGA; the cells that co-expressed IFN-α and IFN-λ were the cells with the highest levels of IFN-α expression. Antibody cross-linking of CD4 or BDCA-2 molecules on pDC inhibited both HSV-induced IFN-λ and IFN-α production. Like the production of IFN-α, the HSV-induced IFN-λ production in pDC was mediated through TLR9 and independent of virus replication. Exogenous IFN-λ treatment of pDC resulted in increased virus-induced expression of both IFN-α and IFN-λ. In addition, both exogenous IFN-λ and –α inhibited dexamethasone-induced apoptosis of pDC. We conclude that pDC are major producers of IFN-λ1 and –λ2 in response to viral stimulation and also express functional receptors for this cytokine. Thus, IFN-λ can serve as an autocrine signal to strengthen the antiviral response of pDC by increasing IFN-α and IFN-λ production, resulting in prolonged pDC survival.

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