Immune response associated with ischemia and reperfusion injury during organ transplantation

Abstract

Background Ischemia and reperfusion injury (IRI) is an ineluctable immune-related pathophysiological process during organ transplantation, which not only causes a shortage of donor organs, but also has long-term and short-term negative consequences on patients. Severe IRI-induced cell death leads to the release of endogenous substances, which bind specifically to receptors on immune cells to initiate an immune response. Although innate and adaptive immunity have been discovered to play essential roles in IRI in the context of organ transplantation, the pathway and precise involvement of the immune response at various stages has not yet to be elucidated. Methods We combined “IRI” and “organ transplantation” with keywords, respectively such as immune cells, danger signal molecules, macrophages, neutrophils, natural killer cells, complement cascade, T cells or B cells in PubMed and the Web of Science to search for relevant literatures. Conclusion Comprehension of the immune mechanisms involved in organ transplantation is promising for the treatment of IRI, this review summarizes the similarities and differences in both innate and adaptive immunity and advancements in the immune response associated with IRI during diverse organ transplantation.

Mechanisms of Cold Preservation and Reperfusion Injury for Solid Organ Transplantation: Implications for Partial Heart Transplantations

“…CD4+ T cells have repeatedly been shown in animal studies to play an integral role in facilitating donor organ inflammation and damage following transplantation through cytokine secretion and a CD154 and CD40-mediated process [49,50]. CD4+ T cell activation leads to differentiation into Th1, Th2, Th17, and Treg cell lineages, which each play unique roles in the immune response [51,52]. Th1 and Th17 have been shown to cause a pro-inflammatory environment in the post-transplant milieu promoting tissue damage and rejection.…”

Modulatory immune responses in fungal infection associated with organ transplant - advancements, management, and challenges

“…Hypoxia, ischemia, and microcirculation are critical factors influencing fungal infections in grafts, particularly in organ transplantation. These factors contribute to the local tissue environment and can significantly impact the ability of the graft to resist fungal infections ( 183 – 186 ). Understanding their roles is essential to manage fungal infection risks in transplanted organs effectively.…”

“…Grafts subjected to ischemia are more vulnerable to fungal infections due to their compromised blood flow, which restricts the delivery of oxygen and nutrients to the site of infection. Furthermore, the diminished oxygen levels in ischemic grafts weaken the host’s defense mechanisms, making it easier for fungal pathogens to colonize and thrive within the graft ( 184 , 186 ). Microcirculation, comprising blood flow through the smallest blood vessels, including capillaries, plays a vital role in delivering oxygen and nutrients to tissues.…”

Ultrasmall Nanoparticles Regulate Immune Microenvironment by Activating IL‐33/ST2 to Alleviate Renal Ischemia‐Reperfusion Injury

“…[ 22 ] The effector T cells can produce pro‐inflammatory cytokines to aggravate kidney injury. [ 23 ] However, regulatory T (Treg) cells possess a negative immune regulation function, and are able to inhibit effector T cells by releasing the anti‐inflammatory cytokine IL‐10, which suppresses the overactive immune inflammatory response. [ 24 ] It has been demonstrated that the cytokine‐mediated expansion of Treg cells can inhibit the inflammatory response to alleviate renal IRI.…”