Introduction. The advances in cerebral ischemia treatment have resulted in a larger proportion of patients get the benefits of rebuilding blood flow to the brain. Then, ischemia-reperfusion injury has emerged as a new essential problem. Dectin-1 plays an important role in cerebral ischemia-reperfusion injury by regulating the function of immune cells. Methods. C57BL/6 was blindly divided into four groups including the sham-operated group and the three different kinds of middle cerebral artery occlusion (MCAO) groups (after 6 hours, 12 hours, and 24 hours after plug removal). The protein expression levels of dectin-1, proapoptosis molecule, and antiapoptosis molecule were measured by using western blot analysis. The brain tissue was analyzed by flow cytometry to detect the M1 macrophage levels. Results. The correlation analysis of dectin-1 and infarct areas showed that there was an obviously positive correlation in between them (R = 0.9603). Dectin-1, cleaved caspase-3, and Bax increased, while antiapoptosis molecule, Bcl-2, decreased at three appropriate time points (after 6 hours, 12 hours, and 24 hours). The level of M1 macrophages in the experimental group increased after ischemia-reperfusion injury compared to the control group. Conclusions. The high expression level of dectin-1 may affect M1 macrophage polarization and brain cell apoptosis in cerebral ischemia-reperfusion injury.

Class II transactivator (CIITA) is a master regulator of MHC gene expression and plays a role in inducing the expression of other immune system genes, including IL‐4, IL‐10 and Fas ligand, as well as more than 60 other immunologically significant genes. We used CIITA as a candidate gene to analyse whether any single‐nucleotide polymorphisms (SNPs) are associated with chronic hepatitis B virus (HBV) infection. In total, 773 patients with chronic HBV infection were enrolled in this hospital‐based case–control study. The patients were divided into groups according to their clinical characteristics: 596 patients had chronic hepatitis B (CHB), and 177 patients had hepatocellular carcinoma (HCC). A total of 313 patients with self‐limited HBV infection were selected as the control group. CIITA gene variants were screened using Haploview 4.2 software; improved multiplex ligation detection reaction technology was then used for genotype detection, and HaploReg v4.1 was employed to predict the functions of 15 variants. The results showed that SNPs in introns in the CIITA gene, namely, rs13333382 (TT + TA vs. AA: p = .003, odds ratio (OR) = 0.65, 95% confidence interval (CI) = 0.49–0.87) and rs4780335 (CC + CG vs. GG: p = 9.40 × 10−5, OR = 0.55, 95% CI = 0.41–0.74), were positively associated with self‐limited HBV infection in the dominant genetic model. Additionally, SNP rs1139564 (TT + TC vs. CC: p = .002, OR = 1.61, 95% CI = 1.19–2.16) in the 3' untranslated region may increase the risk of CHB. According to in silico analysis, all three statistically significant variants act as transcription factor binding motifs. However, we did not find that these 15 mutations are associated with HCC risk. Therefore, we believe that CIITA is a susceptibility gene for CHB rather than for HCC.