Renal allograft fibrosis has been the key pathological characteristic of chronic allograft nephropathy (CAN), which is the major cause of graft loss in renal transplant recipients. The pathogenesis of CAN is complex and incompletely understood, which is the long-term result of immunological and non-immunological injury, including acute rejection episodes, hypoperfusion, ischemia-reperfusion, calcineurin toxicity, infection, and recurrent disease. Highly effective treatment of CAN remains scarce and multidisciplinary strategies are needed. Recent evidence of alloimmunity in renal allograft injury, especially in the complement system, innate immune cells, antibody-mediated rejection, and tolerance induction, suggests the close correlation between acute immunological events and renal allograft fibrosis. These recent findings painted a fascinating and incomplete picture of early detection and treatment targeting acute immune response, which may slow the progression of late injury and renal allograft injury. Thus, we need to have a detailed understanding of the acute and late phase immunological events in disease pathogenesis, especially in the context of oxidative stress, antibody-mediated vascular injury, immune activation, and inflammation leading to renal allograft fibrosis, as well as its related immunotherapy.
This Research Topic aims to discuss the role of alloimmunity in renal allograft fibrosis, and the immunotherapy targeting fibrosis in the light of the most recent findings. All types of contributions that clarify novel mechanisms or new interpretations of well-known mechanisms are welcome. These include microenvironment crosstalk in the allograft, immune cells activity and cytokine production, onset and impact of alloantibody, and the role of chronic inflammation. A particular point of interest will be the works that address the long-term survival of allograft and recipients, which provide new insights for clinical practice and disease management. Manuscripts from the following subtopics on renal allograft are also welcome:
1) Antibody-mediated vascular injury
2) Human and/or veterinary clinical trials using immunotherapy against fibrosis
3) Innate immunity activation and chronic inflammation
4) Personalized detection and therapy targeting alloimmunity
5) Infection disease in renal allograft
Renal allograft fibrosis has been the key pathological characteristic of chronic allograft nephropathy (CAN), which is the major cause of graft loss in renal transplant recipients. The pathogenesis of CAN is complex and incompletely understood, which is the long-term result of immunological and non-immunological injury, including acute rejection episodes, hypoperfusion, ischemia-reperfusion, calcineurin toxicity, infection, and recurrent disease. Highly effective treatment of CAN remains scarce and multidisciplinary strategies are needed. Recent evidence of alloimmunity in renal allograft injury, especially in the complement system, innate immune cells, antibody-mediated rejection, and tolerance induction, suggests the close correlation between acute immunological events and renal allograft fibrosis. These recent findings painted a fascinating and incomplete picture of early detection and treatment targeting acute immune response, which may slow the progression of late injury and renal allograft injury. Thus, we need to have a detailed understanding of the acute and late phase immunological events in disease pathogenesis, especially in the context of oxidative stress, antibody-mediated vascular injury, immune activation, and inflammation leading to renal allograft fibrosis, as well as its related immunotherapy.
This Research Topic aims to discuss the role of alloimmunity in renal allograft fibrosis, and the immunotherapy targeting fibrosis in the light of the most recent findings. All types of contributions that clarify novel mechanisms or new interpretations of well-known mechanisms are welcome. These include microenvironment crosstalk in the allograft, immune cells activity and cytokine production, onset and impact of alloantibody, and the role of chronic inflammation. A particular point of interest will be the works that address the long-term survival of allograft and recipients, which provide new insights for clinical practice and disease management. Manuscripts from the following subtopics on renal allograft are also welcome:
1) Antibody-mediated vascular injury
2) Human and/or veterinary clinical trials using immunotherapy against fibrosis
3) Innate immunity activation and chronic inflammation
4) Personalized detection and therapy targeting alloimmunity
5) Infection disease in renal allograft
