About this Research Topic
Chronic rejection (CR) remains a leading cause of graft dysfunction in transplantation, and the etiology and pathogenesis underlined are still not completely understood. CR is considered to be the principal factor affecting long term graft or patient survival in most cases. The manifestation of CR is mainly characterized by the graft vasculopathy, accompanied with myointimal proliferation, interstitial inflammation, damage of parenchymal cells, interstitial fibrosis, and progressive narrowing of the arterial lumen, resulting in ischemic changes of the allografts, fibrosis, dysfunction, and graft loss.
While it is known that CR is mainly due to an alloimmune response to the allograft, the pathogenesis remains elusive and has not been well characterized. Antibody mediated rejection is considered to be a major mechanism associated with CR. Stem cells or regenerative cells have been recently proposed as promising “live” drugs, being able to target the anti-recipient immune response and prolong allograft survival. At present, although the current immunosuppressive therapies such as calcineurin inhibitors have significantly prolonged the short-term transplant survival, the remaining persistent immune and inflammatory responses to the allo-MHC mismatched allografts have not been fully understood.
The goal of this Research Topic is to focus on the latest advances in the understanding of the pathophysiology and immunopathogenesis of the chronic graft rejection, by which we may be able to develop novel therapeutic interventions to prevent or treat the chronic graft rejection, resulting in further prolongation of graft survival.
We welcome submissions of Original Research, Review, Mini-Review, Clinical Trials, as well as Case Reports focusing on the following subtopics:
- Cellular and molecular mechanisms in the development of chronic allograft vasculopathy
- Cellular and molecular aspects of the chronic immune responses to alloantigens
- Cellular and molecular mechanisms of graft tissue fibrosis
- New immunotherapies for the prevention of chronic vasculopathy and tolerance induction
- Stem cells or regenerative cells in immunomodulation
While it is known that CR is mainly due to an alloimmune response to the allograft, the pathogenesis remains elusive and has not been well characterized. Antibody mediated rejection is considered to be a major mechanism associated with CR. Stem cells or regenerative cells have been recently proposed as promising “live” drugs, being able to target the anti-recipient immune response and prolong allograft survival. At present, although the current immunosuppressive therapies such as calcineurin inhibitors have significantly prolonged the short-term transplant survival, the remaining persistent immune and inflammatory responses to the allo-MHC mismatched allografts have not been fully understood.
The goal of this Research Topic is to focus on the latest advances in the understanding of the pathophysiology and immunopathogenesis of the chronic graft rejection, by which we may be able to develop novel therapeutic interventions to prevent or treat the chronic graft rejection, resulting in further prolongation of graft survival.
We welcome submissions of Original Research, Review, Mini-Review, Clinical Trials, as well as Case Reports focusing on the following subtopics:
- Cellular and molecular mechanisms in the development of chronic allograft vasculopathy
- Cellular and molecular aspects of the chronic immune responses to alloantigens
- Cellular and molecular mechanisms of graft tissue fibrosis
- New immunotherapies for the prevention of chronic vasculopathy and tolerance induction
- Stem cells or regenerative cells in immunomodulation
Keywords: Chronic rejection, Antibody-mediated allograft rejection, Stem cells/regenerative cells, Allograft tolerance, Immunosuppression
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.
