Additionally, we demonstrated that IL-33−/− mice were more sensitized to ConA hepatic injury

than WT controls, in agreement with a protective effect of IL-33/ST2 axis in ConA-hepatitis.10 Our findings are closer to earlier data describing an increased tendency of liver injury in IL-33−/− mice42; however, we speculate that IL-33 may not be implicated in death cascade; rather, it is expressed/released by dying cells as a readout marker to justify its proposed “alarmin” functions during necrosis.43 Finally, we primed the CD1d−/− mice that are deficient in NKT cells by ConA injection along with a simultaneous injection of rm-TRAIL. Previously, it has been reported that an abundant amount (i.e., nearly 500 μg/mouse) of rm-TRAIL injected into mice is

necessary this website to induce moderate liver injury.24 In our present work, the injection of only 30 μg/mouse of rm-TRAIL (i.e., 10 times less than used earlier) was sufficient to trigger severe ConA-induced hepatitis in CD1d−/− primed mice. Interestingly, the reconstitution of TRAIL in CD1d−/− mice induced liver IL-33 expression, which was localized in hepatocytes. We stimulated primary hepatocytes in vitro with rm-TRAIL in order to exclude an indirect effect of TRAIL on IL-33 expression during ConA-induced liver injury. Interestingly, TRAIL readily induced IL-33 expression in cultured murine hepatocytes. In conclusion, our http://www.selleckchem.com/products/BKM-120.html work demonstrates MCE that the molecular regulation of IL-33 in hepatocytes during acute hepatitis is not dependent on FasL or TNFα, but on TRAIL. For immunohistochemistry analysis and animal house facilities, the authors thank the dedicated platforms (i.e., H2P2, ImPACell, and animal house platforms) of SFR BIOSIT, University of Rennes 1, France. Additional Supporting Information may be found

in the online version of this article. “
“I read with great interest the article by Rein et al.1 In this manuscript, the authors attempt to address the prevalence of hepatitis B surface antigen (HBsAg) in foreign-born persons living in the United States. The authors did so by requesting data on hepatitis B screening from refugee health coordinators around the country. The authors indicate that estimates for HBsAg prevalence from the study correspond to estimates from the literature for each country (where comparison is available). One should be very careful when extrapolating the findings of one group of refugees to an entire nation. Generally, refugees that enter one jurisdiction come from the same area in the country of origin. In sub-Saharan Africa, rates of hepatitis B virus (HBV) for each country vary according to regional areas; this is likely related to the habits and customs of each region within a country. The authors report a prevalence of HBsAg of 3.1% in refugees from Tanzania. The rates of HBsAg for Tanzania range from 4.