Research Progress

New progress on treating inflammatory diseases

Date:04-12-2015   |   【Print】 【close

Inflammatory response plays significant roles in human body’s resistance outside pathogen invading, repair of tissue and adjustment of stress response. In pathology state, abnormal inflammatory response relates closely to a variety of diseases. Hepatocellular carcinoma (HCC) has become a major public health problem in China, which is frequently associated with pathogen infection–induced chronic inflammation. Large numbers of innate immune cells are present in HCCs and can influence disease outcome.

Recently, the researchers joined hands with 2 teams headed by Prof. Bin Wei in WIV and Prof. Hongyan Wang in Shanghai Institutes for Biological Sciences, and got important headways in treating inflammatory diseases and dendritic cells vaccine. First, they have demonstrated that the tumor suppressor serine/threonine-protein kinase 4 (STK4) differentially regulates TLR3/4/9-mediated inflammatory responses in macrophages and thereby is protective against chronic inflammation–associated HCC, which suggests that STK4 has potential as a diagnostic biomarker and therapeutic target for inflammation-induced HCC.

Besides, by measuring serum levels of inflammatory biomarkers along with lipid and nutritional parameters in 53 patients who suffered different degrees of particularly peripheral artery stenosis (PAS), they have found serum concentrations of vascular endothelial growth factor-c (VEGF-C) and IL-6 (Interleukin 6) were significantly increased in patients showing moderate or severe PAS. Furthermore, the number of blood monocytes from PAS patients was significantly increased, which showed elevated adhesion to plate-coated fibrinogen. The study suggests that serum concentrations of VEGF-C and IL-6 might be used as biomarkers for diagnosis severe PAS in combination with clinical imaging examination.

Additionally, in the aspect of treating inflammatory diseases, they have identified that ADAP and SKAP55 can enhance PD1 expression via the transcription factor NFATc1 in CD8+ CTL s (cytotoxic T lymphoc-ytes), and proposed that targeting the unrecognized ADAPSKAP55NFATc1PD1 pathway might increase efficacy of antitumor immunotherapy.