Department of Surgery, Starzl Transplantation Institute, University of Pittsburgh School of Medicine, 200 Lothrop Street, W1540 BST, Pittsburgh, PA 15261, USA.
Immunol Res. 2011 Aug;50(2-3):221-7. doi: 10.1007/s12026-011-8223-0.
In the steady state, hepatic antigen (Ag)-presenting cells (APC) generally dampen systemic inflammatory responses to gut-derived Ags. Our studies focus on the role of specific liver APC populations, both non-parenchymal cells (dendritic cells [DC], Kupffer cells, and hepatic stellate cells [HSC]) and parenchymal cells, in the molecular regulation of tissue damage (ischemia and reperfusion [I/R] injury) and immunity following liver transplantation. We focus on factors that either promote or overwhelm the natural tendency of the liver to suppress inflammatory/immune responses. We are also examining molecular mechanisms that regulate liver DC maturation and function and that determine their role in the control of allogeneic T-cell function and the fate of the transplanted liver. Our studies are also aimed at elucidating mechanisms by which HSC regulate DC and T-cell function. These investigations may provide new targets for therapeutic intervention in liver inflammation.
在稳定状态下，肝脏抗原（Ag）呈递细胞（APC）通常会抑制肠道来源的Ag 引起的全身炎症反应。我们的研究集中在特定的肝 APC 群体的作用上，包括非实质细胞（树突状细胞[DC]、枯否细胞和肝星状细胞[HSC]）和实质细胞，在肝移植后组织损伤（缺血再灌注[I/R]损伤）和免疫的分子调节中。我们关注的是促进或压倒肝脏抑制炎症/免疫反应的自然趋势的因素。我们还在研究调节肝 DC 成熟和功能的分子机制，并确定它们在控制同种异体 T 细胞功能和移植肝命运中的作用。我们的研究还旨在阐明 HSC 调节 DC 和 T 细胞功能的机制。这些研究可能为肝脏炎症的治疗干预提供新的靶点。
