Kidney disease is a leading cause of death worldwide and is increasingly recognized as a global health problem. The kidneys are a frequent target of systemic immune and autoimmune disorders, including systemic autoimmunity and vasculitis, immune complex-related serum sickness, and complement disorders. The complex regulation between the immune system and inflammation plays a key role in the progression of kidney disease, especially in immune-related nephropathy. Cytokines released by monocytes/macrophages, including IL-17, INF-γ, TNF, and IL-6, exacerbate renal dysfunction and injury. M1 pro-inflammatory cells help to clear infections but can also promote renal injury and lead to renal fibrosis. Loss of immune homeostasis can exacerbate the adverse effects of inflammation on the kidney and lead to loss of renal function. Therefore, further understanding of immune dysregulation and inflammatory responses has the potential to develop innovative, paradigm-shifting strategies for the treatment of kidney disease. The development of novel computational tools and genomic data analysis are accelerating our understanding of the crosstalk of immunity and inflammation in kidney disease.The aim of this Research Topic is to provide a forum to explore potential and effective therapeutic targets by focusing on the role of regulatory mechanisms of immunity and inflammation in renal disease. We aim to elucidate the possible biological mechanisms of immunity and inflammation in the pathogenesis of kidney disease.We welcome submissions of Original Research and Review articles, including but not limited to the following: (1) The role of immune regulation of inflammation in immune-related nephropathy.(2) Mechanisms of immune and inflammatory interactions in hypertensive nephropathy.(3) Emerging novel cytokines and immune markers in the diagnosis and prognosis of membranous nephropathy.(4) Pathogenetic mechanism of inflammation in chronic kidney disease.(5) Influence of chemokines and chemokine receptors on inflammation in kidney disease.
Kidney disease is a leading cause of death worldwide and is increasingly recognized as a global health problem. The kidneys are a frequent target of systemic immune and autoimmune disorders, including systemic autoimmunity and vasculitis, immune complex-related serum sickness, and complement disorders. The complex regulation between the immune system and inflammation plays a key role in the progression of kidney disease, especially in immune-related nephropathy. Cytokines released by monocytes/macrophages, including IL-17, INF-γ, TNF, and IL-6, exacerbate renal dysfunction and injury. M1 pro-inflammatory cells help to clear infections but can also promote renal injury and lead to renal fibrosis. Loss of immune homeostasis can exacerbate the adverse effects of inflammation on the kidney and lead to loss of renal function. Therefore, further understanding of immune dysregulation and inflammatory responses has the potential to develop innovative, paradigm-shifting strategies for the treatment of kidney disease. The development of novel computational tools and genomic data analysis are accelerating our understanding of the crosstalk of immunity and inflammation in kidney disease.The aim of this Research Topic is to provide a forum to explore potential and effective therapeutic targets by focusing on the role of regulatory mechanisms of immunity and inflammation in renal disease. We aim to elucidate the possible biological mechanisms of immunity and inflammation in the pathogenesis of kidney disease.We welcome submissions of Original Research and Review articles, including but not limited to the following: (1) The role of immune regulation of inflammation in immune-related nephropathy.(2) Mechanisms of immune and inflammatory interactions in hypertensive nephropathy.(3) Emerging novel cytokines and immune markers in the diagnosis and prognosis of membranous nephropathy.(4) Pathogenetic mechanism of inflammation in chronic kidney disease.(5) Influence of chemokines and chemokine receptors on inflammation in kidney disease.