Abstract
Pediatric post-transplant idiopathic liver fibrosis is an unexplained graft fibrosis that occurs in symptom-free children without acute rejection and surgical complications. Despite a lack of consensus on the subject, the development of pediatric post-transplant idiopathic liver fibrosis is believed to be the result of multiple potential factors, including ischemia-reperfusion injury, allogeneic acute and chronic rejection, viral hepatitis recurrence, opportunistic infection, and drug-induced liver damage. Among them, there is growing evidence that innate immunity may also have a unique role in this progression. This study reviews the features of pediatric post-transplant idiopathic liver fibrosis and discusses current studies illustrating the potential mechanisms of liver allograft tolerance induced by intrahepatic innate immunity, the role of components including Toll-like receptors (TLRs), interferons (IFN), dendritic cells (DC), natural killer cells (NK cells), NKT cells, neutrophils, and Kupffer cells, as well as their possibly relevant role in the development of pediatric post-transplant idiopathic liver fibrosis.
Highlights
Pediatric liver transplantation is one of the most effective choices of treatment for many advanced liver diseases in children
We examine the role of some essential components in innate immunity and its possible role in the development of pediatric post-transplant idiopathic liver fibrosis
When it comes to immunosuppressive therapy after liver transplantation, a study by Lee et al demonstrated that intracellular processing events of antigens by dendritic cells (DC) are partly inhibited by tacrolimus and cyclosporine A(CsA), two commonly used immunosuppressants post-surgery [44]
Summary
Pediatric liver transplantation is one of the most effective choices of treatment for many advanced liver diseases in children. Most pediatric primary liver diseases can be cured through liver transplantation, the incidence of post-transplant idiopathic liver fibrosis is extremely high in this population [1,2,3]. As liver fibrosis progresses to cirrhosis, the life quality of patients deteriorates gradually, whereas a long-term study by Venturi reported that liver function of 70% pediatric recipients with graft fibrosis has been maintained within an acceptable fluctuation range. It has been proved that innate immunity plays a crucial part in immune intolerance after graft transplantation and in liver fibrosis, while the detailed mechanism remains unclear in pediatric post-transplant idiopathic liver fibrosis. We examine the role of some essential components in innate immunity and its possible role in the development of pediatric post-transplant idiopathic liver fibrosis
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