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- W4313350089 abstract "Abstract Replication-defective recombinant Adenoviruses are potential innovative viral vaccine vectors for treating many inherited and acquired human diseases. Broad clinical application of Adenoviruses in vaccine development is being hindered by the induction of vigorous innate and adaptive immune responses against the vector resulting in loss of Adenovirus transgene and deleterious effects in the liver. Vα14iNKT cells are thymic-derived innate T cells at the interface between the two arms of the immune response. The pathophysiological role of Vα14iNKT cells during replication-defective Adenovirus infection is not known, and is therefore a focus of our study. Our results revealed that Vα14iNKT cells were activated in response to Adenovirus infection to produce hepatic CCL5. In vivo studies utilizing CCL5 deficient mice showed that CCL5 deficiency caused reduced liver pathology and Adenovirus transgene loss. Similar results were also seen after blocking the biological effects of CCL5 receptors. Additionally, our data also revealed a novel and previously unrecognized pro-inflammatory role for activated intrahepatic Vα14iNKT cells in promoting liver pathology by positively regulating intrahepatic γδT cell activation. In summary, we have identified a novel and important pro-inflammatory role for activated intrahepatic Vα14iNKT cells in positively regulating both hepatic CCL5 and activated intrahepatic γδT cells to induce liver pathology without loss of Adenovirus transgene." @default.
- W4313350089 created "2023-01-06" @default.
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- W4313350089 date "2010-04-01" @default.
- W4313350089 modified "2023-09-27" @default.
- W4313350089 title "Intrahepatic Vα14iNKT cells Promote Liver Pathology during Adenovirus infection by Regulating Hepatic CCL5 and Intrahepatic γδT cell Activation: Implications for Vaccine Development (89.2)" @default.
- W4313350089 doi "https://doi.org/10.4049/jimmunol.184.supp.89.2" @default.
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