Human IL-18R1 ELISA Kit

The interleukin 18 receptor (IL18R1) gene is a strong candidate gene for sthma. It has been implicated in the pathophysiology of asthma and maps to an asthma susceptibility locus on chromosome 2q12. The possibility of association between polymorphisms in IL18R1 and asthma was examined by genotyping seven SNPs in 294, 342 and 100 families from Denmark, United Kingdom and Norway and conducting family-based association analyses for asthma, atopic asthma and bronchial hyper-reactivity (BHR) phenotypes. Three SNPs in IL18R1 were associated with asthma (0.01131 <= P <= 0.01377), five with atopic asthma (0.00066 <= P <= 0.00405) and two with BHR (0.01450 <= P <= 0.03203) in the Danish population; two SNPs were associated with atopic asthma (0.00397 <= P <= 0.01481) and four with BHR (0.00435 <= P <= 0.03544) in the UK population; four SNPs showed associations with asthma (0.00015 <= P <= 0.03062), two with atopic asthma (0.01269 <= P <= 0.04042) and three with BHR (0.00259 <= P <= 0.01401) in the Norwegian population; five SNPs showed associations with asthma (0.00005 <= P <= 0.03744), five with atopic asthma (0.00001 <= P <= 0.04491) and three with BHR (0.03568 <= P <= 0.04778) in the combined population. Three intronic SNPs (rs1420099, rs1362348 and rs1974675) showed replicated association for at least one asthma-related phenotype. These results demonstrate significant association between polymorphisms in IL18R1 and asthma.

Chronic inflammation in liver tissue is an underlying cause of hepatocellular carcinoma. High levels of inflammatory cytokine IL18 in the circulation of patients with hepatocellular carcinoma correlates with poor prognosis. However, conflicting results have been reported for IL18 in hepatocellular carcinoma development and progression. In this study, we used tissue specimens from hepatocellular carcinoma patients and clinically relevant mouse models of hepatocellular carcinoma to evaluate IL18 expression and function. In a mouse model of liver fibrosis that recapitulates a tumor-promoting microenvironment, global deletion of the IL18 receptor IL18R1 enhanced tumor growth and burden. Similarly, in a carcinogen-induced model of liver tumorigenesis, IL18R1 deletion increased tumor burden. Mechanistically, we found that IL18 exerted inflammation-dependent tumor-suppressive effects largely by promoting the differentiation, activity, and survival of tumor-infiltrating T cells. Finally, differences in the expression of IL18 in tumor tissue versus nontumor tissue were more predictive of patient outcome than overall tissue expression. Taken together, our findings resolve a long-standing contradiction regarding a tumor-suppressive role for IL18 in established hepatocellular carcinoma and provide a mechanistic explanation for the complex relationship between its expression pattern and hepatocellular carcinoma prognosis. (C) 2016 AACR.