About this Research Topic
This Research Topic is the second volume of the “Community Series in Hepatic Immune Response underlying Liver Cirrhosis and Portal Hypertension”. Please see the first volume here.
Liver cells include hepatocytes, cholangiocytes, liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs), Kupffer cells, NK cells, neutrophils, T and B cells. In healthy conditions, the liver is a critical immunological organ by maintaining homeostatic cellular interactions. Under various etiological stimulations, such as alcohol, viruses, Western diet, endotoxins from the gut microbiota, and circulating antigens, the hepatic immune homeostasis is disrupted leading to chronic liver diseases and eventually liver cirrhosis and/or hepatocellular carcinoma (HCC). The mechanisms of liver cirrhosis are complex, involving different cells, signaling pathways, and the liver microenvironment. Although great advances have been made in preventing liver diseases, the worldwide morbidity and mortality of liver cirrhosis remain high. Portal hypertension and portal vein thrombosis are the leading causes of cirrhosis-related death. HSCs have been recognized as the primary effector cell in the fibrotic liver. The accumulation of ECM produced by HSC activation leads to increased fibrotic septa and hepatic resistance, and eventually, the development of liver cirrhosis and portal hypertension. Recently, LSECs, macrophage, neutrophils, sinusoidal communication, and hepatic immune response has been demonstrated to play a critical role in developing liver cirrhosis and portal hypertension. The abnormal hepatic immune response and disturbed immune homeostasis might lead to HSC activation and dysfunctional sinusoidal communication. However, the molecular and cellular mechanisms underlying the hepatic immune response in liver cirrhosis and portal hypertension remain unclear.
The present Research Topic aims to report the most recent advances in uncovering the immune mechanisms underlying liver cirrhosis and portal hypertension. The topic will be open to Reviews, Original Research Articles, and Clinical Trial articles that focus on, but are not limited to, the following themes:
1. Novel mechanisms of hepatic immune response in liver cirrhosis and its complications
2. New cellular interactions in liver cirrhosis.
3. Novel therapeutic targets and pharmacological regulation of hepatic immune response in liver cirrhosis.
4. Metabolism and immune response in liver cirrhosis.
5. Role of the gut-liver axis in the development of liver cirrhosis.
6. Clinical trials related to the immune response in liver cirrhosis
7. New immunotherapy and immune cell-based therapy in liver cirrhosis.
Liver cells include hepatocytes, cholangiocytes, liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs), Kupffer cells, NK cells, neutrophils, T and B cells. In healthy conditions, the liver is a critical immunological organ by maintaining homeostatic cellular interactions. Under various etiological stimulations, such as alcohol, viruses, Western diet, endotoxins from the gut microbiota, and circulating antigens, the hepatic immune homeostasis is disrupted leading to chronic liver diseases and eventually liver cirrhosis and/or hepatocellular carcinoma (HCC). The mechanisms of liver cirrhosis are complex, involving different cells, signaling pathways, and the liver microenvironment. Although great advances have been made in preventing liver diseases, the worldwide morbidity and mortality of liver cirrhosis remain high. Portal hypertension and portal vein thrombosis are the leading causes of cirrhosis-related death. HSCs have been recognized as the primary effector cell in the fibrotic liver. The accumulation of ECM produced by HSC activation leads to increased fibrotic septa and hepatic resistance, and eventually, the development of liver cirrhosis and portal hypertension. Recently, LSECs, macrophage, neutrophils, sinusoidal communication, and hepatic immune response has been demonstrated to play a critical role in developing liver cirrhosis and portal hypertension. The abnormal hepatic immune response and disturbed immune homeostasis might lead to HSC activation and dysfunctional sinusoidal communication. However, the molecular and cellular mechanisms underlying the hepatic immune response in liver cirrhosis and portal hypertension remain unclear.
The present Research Topic aims to report the most recent advances in uncovering the immune mechanisms underlying liver cirrhosis and portal hypertension. The topic will be open to Reviews, Original Research Articles, and Clinical Trial articles that focus on, but are not limited to, the following themes:
1. Novel mechanisms of hepatic immune response in liver cirrhosis and its complications
2. New cellular interactions in liver cirrhosis.
3. Novel therapeutic targets and pharmacological regulation of hepatic immune response in liver cirrhosis.
4. Metabolism and immune response in liver cirrhosis.
5. Role of the gut-liver axis in the development of liver cirrhosis.
6. Clinical trials related to the immune response in liver cirrhosis
7. New immunotherapy and immune cell-based therapy in liver cirrhosis.
Keywords: #CollectionSeries, Hepatic, Immunity, Immune response, Liver, Cirrhosis, Hypertension
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
