Modulierung spezifischer T Zellantworten gegen das Hepatitis B Virus (HBV) durch PRRs (TLR2 und -13) und PRR Detektion der HBV Infektion (B05)

该项目的重点是TLR2在HBV传感和TLR2配体驱动的HBV特异性T细胞应答中的作用。TLR2配体激活肝脏中的LSEC以促进针对HBV的局部T细胞应答。由此产生的肝内T细胞应答在小鼠模型中有效介导HBV清除。PI将研究TLR 2介导的HBV特异性T细胞活化的分子机制，以及如何在肝脏环境中优化其功能和存活。这将在动物模型（小鼠，土拨鼠）和HBV感染个体的患者样本中进行测试。他们还将分析肉豆蔻酰化HBsAg是否是HBV感染期间起作用的TLR2配体。将在慢性HBV感染的小鼠模型中分析HBsAg驱动的肝内Treg应答的潜在机制。

Project focuses on the role of TLR2 in HBV sensing and TLR2 ligand driven HBV-specific T cell responses. TLR2 ligands activate LSECs in the liver to promote local T cell responses against HBV. The resultant intrahepatic T cell response efficiently mediates HBV clearance in mouse models. The PIs will investigate the molecular mechanisms underlying TLR2-mediated activation of HBV-specific T cells and how their function and survival can be optimized in the hepatic environment. This will be tested in animal models (mouse, woodchuck) and patient samples from HBV-infected individuals. They will also analyze whether myristoylated HBsAg is a TLR2 ligand operative during HBV infection. The mechanisms underlying HBsAg driven intrahepatic Treg responses, will be analyzed in mouse models of chronic HBV infection.