About this Research Topic
Innate immunity is a vital defense system in animals and humans, which is regulated precisely. In the immune system, a balance between offensive and defensive actions is crucial to maintain homeostasis. The regulation of innate immunity orchestrated by immune cells and cytokines is of importance in physiological and pathological conditions. Innate immune responses are characterized by the activity of innate immune cells such as neutrophils, macrophages, dendritic cells, and also tubular epithelial cells and endothelial cells.
These innate immune cells not only participate in inflammation after renal insults causing detrimental influence but also play a protective role in the repair post-injury. Over-reactive and persistent immune-inflammatory responses result in tubular injury, mal-repair, and interstitial fibrosis. In addition, the timely and beneficial clearing of damaged cells including apoptotic and necrotic cells is often executed via phagocytosis by neutrophils and macrophages, as well as tubular epithelial cells. Disclosing the complex mechanisms of renal injury and repair, and the orchestrated actions of innate immunity will be beneficial to the intervention strategy of limiting inflammation, promoting repair, and preventing fibrosis in both native and transplant kidneys.
This Research Topic intends to discuss the participation of innate immunity in kidney injury, repair, and fibrosis. The submission of original basic and translational Original Research articles, relevant Review, Mini Review, and Case Reports that cover, but are not limited to, the following subtopics will be encouraged:
1. The role and mechanism of innate immune cells, mediators, and receptors in a variety of acute kidney injury caused by ischemia-reperfusion, as well as acute rejection and immunosuppression in native or transplant kidneys.
2. The involvement of innate immunity in other causes such as sepsis, obstruction, contrast-medium induced acute kidney injury (AKI), or AKI occurred upon chronic kidney diseases, and their related remodeling/recovery or progression/fibrosis.
3. The crucial responses of innate immunity in kidney repair after an initial injury such as phagocytes, phagocytic receptors, phagocytosis, phagosome, damaged cell/debris clearance, in limiting inflammation, and promoting regeneration.
4. The impact of acute kidney injury on the progression of chronic kidney disease and chronic allograft dysfunction, remodeling, or fibrosis through innate immune responses especially related to systemic and local immune cells, their cross-interactions via ligand-receptors，extracellular vesicles or exosomes， as well as related signaling pathways.
5. Therapeutic strategies including gene, protein, and cell therapy for intervening in the balance of innate immunity that inhibits kidney injuries, promote kidney repair, and prevent kidney fibrosis.
These innate immune cells not only participate in inflammation after renal insults causing detrimental influence but also play a protective role in the repair post-injury. Over-reactive and persistent immune-inflammatory responses result in tubular injury, mal-repair, and interstitial fibrosis. In addition, the timely and beneficial clearing of damaged cells including apoptotic and necrotic cells is often executed via phagocytosis by neutrophils and macrophages, as well as tubular epithelial cells. Disclosing the complex mechanisms of renal injury and repair, and the orchestrated actions of innate immunity will be beneficial to the intervention strategy of limiting inflammation, promoting repair, and preventing fibrosis in both native and transplant kidneys.
This Research Topic intends to discuss the participation of innate immunity in kidney injury, repair, and fibrosis. The submission of original basic and translational Original Research articles, relevant Review, Mini Review, and Case Reports that cover, but are not limited to, the following subtopics will be encouraged:
1. The role and mechanism of innate immune cells, mediators, and receptors in a variety of acute kidney injury caused by ischemia-reperfusion, as well as acute rejection and immunosuppression in native or transplant kidneys.
2. The involvement of innate immunity in other causes such as sepsis, obstruction, contrast-medium induced acute kidney injury (AKI), or AKI occurred upon chronic kidney diseases, and their related remodeling/recovery or progression/fibrosis.
3. The crucial responses of innate immunity in kidney repair after an initial injury such as phagocytes, phagocytic receptors, phagocytosis, phagosome, damaged cell/debris clearance, in limiting inflammation, and promoting regeneration.
4. The impact of acute kidney injury on the progression of chronic kidney disease and chronic allograft dysfunction, remodeling, or fibrosis through innate immune responses especially related to systemic and local immune cells, their cross-interactions via ligand-receptors，extracellular vesicles or exosomes， as well as related signaling pathways.
5. Therapeutic strategies including gene, protein, and cell therapy for intervening in the balance of innate immunity that inhibits kidney injuries, promote kidney repair, and prevent kidney fibrosis.
Keywords: kidney injury, repair, fibrosis, phagocyte, monocyte, macrophage, dendritic cell, neutrophil, tubular epithelial cell, endothelial cell, phagocytosis, apoptosis, inflammation, phagocytic receptors, innate immunity, antigen presentation
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