Immune checkpoint inhibitors (ICIs) have emerged as a promising treatment option in the fight against advanced non-small-cell lung cancer (NSCLC). KRAS is the most frequently mutated oncogene in NSCLC. We performed this meta-analysis to investigate if KRAS mutation status affects survival benefits of ICIs in patients with advanced NSCLC. Electronic databases were searched for eligible studies. We included randomized trials with the data of overall survival stratified by KRAS mutation status. From 3 eligible studies, 138 patients with KRAS mutant NSCLC and 371 with KRAS wild-type tumor were included in the meta-analysis. Compared to chemotherapy with docetaxel, ICIs improved overall survival in patients with previously treated KRAS mutant NSCLC (hazard ratio = 0.64 [95% confidence interval, 0.43–0.96], P = 0.03). For patients with KRAS wild-type NSCLC, however, ICIs did not prolong overall survival over that with chemotherapy (hazard ratio = 0.88 [95% confidence interval, 0.68–1.13], P = 0.30). In conclusion, ICIs as a salvage therapy improved overall survival over that with docetaxel in advanced NSCLC patients with KRAS mutation, but not in those with KRAS wild-type tumor. These results suggest that KRAS mutation status may be a potential biomarker for survival benefits to ICIs.

Th17 cells mediate inflammation and autoimmunity. Although it was known that cytokine IL-2 inhibits Th17 cell differentiation, how it does so was elusive. Using IL-17–specific PTEN-deficient mice, Kim et al. show that phosphatase PTEN inhibits IL-2 production and thus promotes Th17 cell differentiation.

Regulatory T (Treg) cells are essential for maintenance of immune homeostasis. Foxp3 is the key transcription factor for Treg-cell differentiation and function; however, molecular mechanisms for its negative regulation are poorly understood. Here we show that YY1 expression is lower in Treg cells than Tconv cells, and its overexpression causes a marked reduction of Foxp3 expression and abrogation of suppressive function of Treg cells. YY1 is increased in Treg cells under inflammatory conditions with concomitant decrease of suppressor activity in dextran sulfate-induced colitis model. YY1 inhibits Smad3/4 binding to and chromatin remodelling of the Foxp3 locus. In addition, YY1 interrupts Foxp3-dependent target gene expression by physically interacting with Foxp3 and by directly binding to the Foxp3 target genes. Thus, YY1 inhibits differentiation and function of Treg cells by blocking Foxp3.

Objective Several recent reviews of published studies have shown that the eradication of H. pylori infection in patients with ITP improved thrombocytopenia in about half of the cases. However, most included studies were observational case series. We performed the first meta-analysis of randomized trials to gain a better insight into the effect of H. pylori eradication in ITP patients. Methods A systematic computerized search of the electronic databases including PubMed, EMBASE, Google Scholar, and Cochrane Library (up to December 2017) was conducted. Results From six studies, a total of 241 patients (125 in eradication group and 116 in control group) were included in the meta-analysis. Patients in the eradication group showed significantly higher overall platelet response rate than those in the control group (odds ratio = 1.93, 95% confidence interval: 1.01–3.71, P = 0.05). In the subgroup analysis, however, children in the eradication group failed to show statistically better response rate than those in the noneradication group (odds ratio = 1.80, 95% confidence interval: 0.88–3.65, P = 0.11). Conclusions This meta-analysis indicates that H. pylori eradication has a significant therapeutic effect in patients with ITP. Considering the intrinsic limits in the design and sample size of the included studies, however, large randomized controlled trials are warranted to validate the therapeutic impact of H. pylori eradication in adults as well as children with ITP.