BackgroundIL-10+ regulatory B (Bregs), CD4+Foxp3+ regulatory T (Tregs), and CD4+CXCR5+Foxp3+ follicular regulatory T (TFR) cells regulate the progression of infection disease. This study aimed at examining how those cells associated with the development of chronic hepatitis B (CHB) and chronic hepatitis C (CHC) in a Chinese population.MethodsThe numbers of circulating IL-10+ Bregs, Tregs and TFR cells in 31 CHC, 58 CHB patients and 22 healthy controls (HC) were examined by flow cytometry. The potential association of those cells with clinical measures was analyzed.ResultsThe numbers of CD5+CD19+CD1dhighIL-10+ Bregs, Tregs and TFR cells and the levels of serum IL-10, IFN-γ and IL-2 in the CHB, and IL-10 and IFN-γ in the CHC patients were significantly higher than that in the HC (p < 0.05). Furthermore, the numbers of circulating IL-10+ Bregs and the levels of serum IL-10, but not other cytokines tested were positively correlated with the levels of serum HBV DNA and ALT in the HBeAg− CHB patients as well as HCV RNA and ALT in CHC patients. Additionally, the numbers of circulating TFR cells were positively correlated with the levels of serum HBV DNA and ALT in the CHB patients as well as HCV RNA and ALT in the CHC patients.ConclusionsIncreased numbers of circulating IL-10+ Bregs and TFR cells are associated with poor virus eradication and liver injury in CHB and CHC patients. Furthermore, the levels of serum IL-10 is associated with the hepatic flares.

Circulating memory T follicular helper subsets, Tfh2 and Tfh17 are found to be aberrantly regulated in many autoimmune diseases. However, their roles in the pathogenesis of GBS are still unclear. This study examined the phenotype, distribution, clinical relevance and potential function of Tfh2 and Tfh17 in 36 GBS patients (including 24 AMAN and 12 AIDP patients). We found that the absolute counts of total memory Tfh cells were significantly increased in AMAN, while no significant difference in AIDP compared with HC. Furthermore, the levels of the three subsets of memory Tfh cells, Tfh1, Tfh2 and Tfh17, were differentially altered in AMAN. The absolute counts of Tfh1, Tfh2 and Tfh17 were all increased to a higher level in AMAN. The ratio of (Tfh2+Tfh17)/Tfh1 and the percentages of ICOS+ cells in Tfh2 and Tfh17 cells were greater in AMAN when compared to AIDP and HC, and the former had a positive correlation with the severity of both AMAN and AIDP. Conversely, the percentages of PD1+ cells in Tfh2 and Tfh17 cells were lower in AMAN than in HC. Therefore, circulating memory Tfh2 and Tfh17 cells might promote the autoantibody-related immune response and serve as useful markers to evaluate the progression of AMAN.

Our results suggest that echinacoside can provide a pronounced protection against GalN/LPS-induced acute liver injury in mice, which may complement the available strategies for management of acute liver damage in clinical settings.

Local anesthetic of bupivacaine may inhibit neurite outgrowth and induce apoptosis in mouse dorsal root ganglia (DRG) neurons. In this work, we intended to investigate the functional role of microRNA 26a (miR-26a) in regulating bupivacaine-induced nerve injury in DRG neurons. DRG neurons were extracted from C57BL/6 mice and cultured in vitro. Bupivacaine was applied in vitro and it induced apoptosis, inhibited neurite growth, and significantly down-regulated miR-26a gene in DRG neurons. MiR-26a mimic was then used to up-regulate miR-26a expression in DRG neurons. We found that miR-26a up-regulation promoted neurite outgrowth and reduced apoptosis in bupivacaine-injured DRG neurons. Luciferase assay and Western blot confirmed that Phosphatase and tensin homolog (PTEN) was down-stream target of miR-26a in DRG neurons. Ectopic PTEN up-regulation was then able to reverse the protective effect of miR-26a overexpression on bupivacaine-induced nerve injury in DRG neurons. Overall, this work demonstrated that miR-26a had a functional role in regulating bupivacaine-induced nerve injury in DRG neurons. Up-regulating miR-26a to suppress PTEN signaling pathway may be an effective method to protect local anesthetic-induced nerve injury in spinal cord.