SummaryT helper type 17 (Th17) cells, which represent a novel subset of CD4 + T cells, play an active role in inflammatory and autoimmune diseases. Recent studies have also suggested that they have an impact on solid tumours. However, the nature of Th17 cells in haematological malignancies remains unknown. In this study, we investigated Th17 cell frequency and secretion of related cytokines in patients with acute myeloid leukaemia (AML). First, we found that Th17 cell frequencies were increased significantly in peripheral blood samples from untreated patients with AML, compared with those from healthy volunteers. Moreover, increased interleukin (IL)-17 concentrations accompanied the increased Th17 cell frequencies in these patients. These results suggest that Th17 cells may play a role in the pathogenesis of AML. Secondly, we found that the increased Th17 cell frequencies were reduced when patients achieved complete remission after chemotherapy, suggesting that measurement of Th17 cell frequencies may have clinical value in the evaluation of therapeutic effect. In addition, we found that IL-6 and transforming growth factor (TGF)-b1 concentrations increased in the untreated patients and that IL-6 concentrations showed a positive correlation with the frequencies of Th17 cells, suggesting that IL-6 may play an important role in Th17 cell differentiation in patients with AML.

The molecular mechanisms of osteoarthritis, the most common chronic disease, remain unexplained. This study aimed to use bioinformatic methods to identify the key biomarkers and immune infiltration in osteoarthritis. Gene expression profiles (GSE55235, GSE55457, GSE77298, and GSE82107) were selected from the Gene Expression Omnibus database. A protein-protein interaction network was created, and functional enrichment analysis and genomic enrichment analysis were performed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) databases. Immune cell infiltration between osteoarthritic tissues and control tissues was analyzed using the CIBERSORT method. Identify immune patterns using the ConsensusClusterPlus package in R software using a consistent clustering approach. Molecular biological investigations were performed to discover the important genes in cartilage cells. A total of 105 differentially expressed genes were identified. Differentially expressed genes were enriched in immunological response, chemokine-mediated signaling pathway, and inflammatory response revealed by the analysis of GO and KEGG databases. Two distinct immune patterns (ClusterA and ClusterB) were identified using the ConsensusClusterPlus. Cluster A patients had significantly lower resting dendritic cells, M2 macrophages, resting mast cells, activated natural killer cells and regulatory T cells than Cluster B patients. The expression levels of TCA1, TLR7, MMP9, CXCL10, CXCL13, HLA-DRA, and ADIPOQSPP1 were significantly higher in the IL-1β-induced group than in the osteoarthritis group in an in vitro qPCR experiment. Explaining the differences in immune infiltration between osteoarthritic tissues and normal tissues will contribute to the understanding of the development of osteoarthritis.

Since the first report in 2005, accumulating interests have been focused on the effect of curcumin in atherosclerosis with discrepancies. Therefore, we conducted a systematic review and meta-analysis to comprehensively estimate its effect against atherosclerosis. Literature search was performed on the database of PubMed, EMBASE, and Cochrane Library to identify relevant studies which estimated the effect of curcumin in atherosclerosis. Reporting effects on aortic lesion area was the primary outcome while effects on serum lipid profiles and circulating inflammatory markers were the secondary outcome. A total of 10 studies including 14 independent pairwise experiments were included in our analysis. We clarified that curcumin could significantly reduce aortic atherosclerotic lesion area (SMD=‐0.89, 95% CI: -1.36 to -0.41, P=0.0003), decrease serum lipid profiles (Tc, MD=‐1.005, 95% CI: -1.885 to -0.124, P=0.025; TG, MD=‐0.045, 95% CI: -0.088 to -0.002, P=0.042; LDL-c, MD=‐0.523, 95% CI: -0.896 to -0.149, P=0.006) as well as plasma inflammatory indicators (TNF-α, MD=‐56.641, 95% CI: -86.848 to -26.433, P<0.001; IL-1β, MD=‐5.089, 95% CI: -8.559 to -1.619, P=0.004). Dose-response meta-analysis predicted effective dosage of curcumin between 0 and 347 mg/kg BW per day, which was safe and nontoxic according to the existing publications. The underlying mechanisms were also discussed and might be associated with the modulation of lipid transport and inflammation in cells within artery walls as well as indirect modulations in other tissues. Clinical evidence from nonatherosclerosis populations revealed that curcumin would lower the lipid profiles and inflammatory responses as it has in a mouse model. However, standard preclinical animal trial designs are still needed; further studies focusing on the optimal dose of curcumin against atherosclerosis and RCTs directly in atherosclerosis patients are also warranted.

These findings demonstrate that blockade of endogenous IL-17 activity by treatment with anti-IL-17 antibody attenuates EAU in rats. IL-17 rather than IFN-gamma plays a crucial role in the development of EAU, and that antagonism of IL-17 could be useful for the treatment of human intraocular autoimmune diseases.