Renal transplantation is currently the optimal therapy for most patients with end-stage renal disease. However, ischemia-reperfusion injury and alloimmune response, the inevitable emergence following transplantation, are well-recognized hurdles of allograft survival. Innate immunity, including innate immune cells, cytokines, and the complement system, plays a vital role in both ischemia-reperfusion injury and rejection. Danger-associated molecular patterns (DAMP) and nonself can be recognized by pattern recognition receptors (PRR), such as toll-like receptors expressed by innate immune cells, contributing to the initiation and maintenance of adaptive immune response. Besides, the complement system is another main inducer of rejection, considering the importance of complement-induced inflammation and endothelial in the pathogenesis of antibody-mediated rejection. Therefore, to improve allograft survival, the knowledge of innate immunity in renal transplantation should be further extended in depth and width.
The goal of this research topic is to explore more novel and valuable knowledge in functions and regulatory mechanisms of innate immunity in renal transplantation especially in ischemia-reperfusion injury and rejection, thus providing promising therapeutic targets and strategies to improve allograft survival.
• Innate immune response and its function in renal transplantation
• Regulatory mechanisms of innate immune cells in renal transplantation
• Homeostasis and differentiation of antigen-presenting cells in renal transplantation
• Metabolism and epigenetic modification in antigen-presenting cells
• The function and mechanisms of complement in rejection of renal transplantation
• Biomarkers related to innate immunity for diagnosis and prognosis of rejection
• Novel therapeutics or agents targeting innate immunity again renal injury and rejection
Renal transplantation is currently the optimal therapy for most patients with end-stage renal disease. However, ischemia-reperfusion injury and alloimmune response, the inevitable emergence following transplantation, are well-recognized hurdles of allograft survival. Innate immunity, including innate immune cells, cytokines, and the complement system, plays a vital role in both ischemia-reperfusion injury and rejection. Danger-associated molecular patterns (DAMP) and nonself can be recognized by pattern recognition receptors (PRR), such as toll-like receptors expressed by innate immune cells, contributing to the initiation and maintenance of adaptive immune response. Besides, the complement system is another main inducer of rejection, considering the importance of complement-induced inflammation and endothelial in the pathogenesis of antibody-mediated rejection. Therefore, to improve allograft survival, the knowledge of innate immunity in renal transplantation should be further extended in depth and width.
The goal of this research topic is to explore more novel and valuable knowledge in functions and regulatory mechanisms of innate immunity in renal transplantation especially in ischemia-reperfusion injury and rejection, thus providing promising therapeutic targets and strategies to improve allograft survival.
• Innate immune response and its function in renal transplantation
• Regulatory mechanisms of innate immune cells in renal transplantation
• Homeostasis and differentiation of antigen-presenting cells in renal transplantation
• Metabolism and epigenetic modification in antigen-presenting cells
• The function and mechanisms of complement in rejection of renal transplantation
• Biomarkers related to innate immunity for diagnosis and prognosis of rejection
• Novel therapeutics or agents targeting innate immunity again renal injury and rejection
