B7-H6 is a ligand of NKp30, which is an activating receptor of natural killer (NK) cells. High expression of B7-H6 is found in certain types of tumor cells, such as lymphoma, leukemia and gastric carcinoma. The expression of B7-H6 can be induced by inflammatory stress in healthy cells. The expression of B7-H6 is significantly correlated with distant metastasis status and post-operative prognosis in cancer patients. The effectiveness of B7-H6 modified antitumor immunotherapy strategies had been verified in tumor-bearing mice, which opened a new door to targeted therapy. In this review, we will focus on the recent development on the roles of B7-H6 in tumor immunity, as well as mechanisms involved in the regulation of B7-H6 expression.
Vascular endothelial cadherin (VE‑cadherin) was first found in vascular endothelial cells to maintain normal vascular structures and regulate endothelial cell permeability by homology adhesion. New evidence indicates that certain invasive tumor cells also express VE‑cadherin, which is involved in vasculogenic mimicry to provide a blood supply required for tumor growth and metastasis. EC1 and EC3 domains of VE‑cadherin were reported to be important for intercellular homology adhesion. In the present study, a monoclonal antibody specific to the outer-membrane immunoglobulin-like domains of VE‑cadherin was generated and the binding epitope was identified as peptide LDREVVPWYNLTVEA in the EC4 domain. This antibody inhibited proliferation and capillary-like structure formation of lung cancer Glc‑82 cells in 3D Matrigel culture in vitro. This effect was mediated by the inhibition of AKT phosphorylation. Our results suggested that the EC4 domain participates in VE‑cadherin clustering and the antibody targeting the EC4 domain of VE‑cadherin may be a promising anti‑vasculogenic mimicry agent for cancer treatment.
Pooled sample testing (PST) as a strategy for avoiding testing the majority of individual negative samples has been proposed for screening of diseases in low prevalence areas. There has been no standard guideline for PST in screening of Schistosoma japonicum infection of Yunnan, China. To document the optimum pool size with acceptable sensitivity of PST for screening of Schistosoma japonicum infection in this setting, an experimental pooling of each of 31 positive sera by IHA with various numbers of 24 negative sera was done. The results were used to create a statistical model which was subsequently used for simulation to predict sensitivity of the pooled serum tests in the population with varying prevalence and pool size. We found that to keep the sensitivity of PST above 90%, 1:05 should be the maximum dilution, that is, the optimum pool size should not be greater than 6. Antigen will have rather little interference if the prevalence of infection is low e.g. 1% or the antigen:antibody ratio is 1:100 or below. Pooled serum testing by IHA is an acceptable sensitive method for detecting antibody for Schistosoma japonicum infection in this area.
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