AI Article Synopsis
- Donor kidneys experience changes in macrophage behavior after ischemia-reperfusion injury, impacting their inflammatory and reparative functions in transplantation.
- Cold ischemia and reversible injury reduce the ability of renal macrophages to present antigens and shift them towards a pro-repair M phenotype while increasing IL-1R8 expression.
- IL-1R8 plays a critical role in regulating macrophage functions post-injury, influencing immune responses and tissue repair, suggesting it could be a potential target for improving transplant outcomes.
Article Abstract
Background: In donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, phagocytes coexpressing the F4/80 and CD11c molecules mediate proinflammatory responses and trigger adaptive immunity in transplantation through antigen presentation. After injury, however, resident renal macrophages coexpressing these surface markers acquire a proreparative phenotype, which is pivotal in controlling inflammation and fibrosis. No data are currently available regarding the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-derived resident renal macrophages to act as professional antigen-presenting cells.
Methods: We evaluated the phenotype and function of intragraft CD11cF4/80 renal macrophages after cold ischemia. We also assessed the modifications of donor renal macrophages after reversible ischemia-reperfusion injury in a mouse model of congeneic renal transplantation. To investigate the role played by IL-1R8, we conducted and studies comparing cells and grafts from wild-type and IL-R8-deficient donors.
Results: Cold ischemia and reversible ischemia-reperfusion injury dampened antigen presentation by renal macrophages, skewed their polarization toward the M phenotype, and increased surface expression of IL-1R8, diminishing activation mediated by toll-like receptor 4. Ischemic IL-1R8-deficient donor renal macrophages acquired an M phenotype, effectively induced IFN and IL-17 responses, and failed to orchestrate tissue repair, resulting in severe graft fibrosis and aberrant humoral immune responses.
Conclusions: IL-1R8 is a key regulator of donor renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phenotype and antigen-presenting role of these cells. It may therefore represent an intriguing pathway to explore with respect to modulating responses against autoantigens and alloantigens after kidney transplant.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7062225 | PMC |
| http://dx.doi.org/10.1681/ASN.2019080778 | DOI Listing |
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