Aiello S, Podestà MA, Rodriguez-Ordonez PY, et al. - Given that phagocytes coexpressing the F4/80 and CD11c molecules mediate proinflammatory responses as well as provoke adaptive immunity in transplantation via antigen presentation in donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, researchers focused on the influences of ischemia-reperfusion injury caused by transplant on the ability of donor-derived resident renal macrophages to behave as professional antigen-presenting cells. They assessed the phenotype as well as the function of intragraft CD11c⁺F4/80⁺ renal macrophages following cold ischemia. The consequences of cold ischemia and reversible ischemia-reperfusion injury included dampening of antigen presentation by renal macrophages, skewing their polarization toward the M₂ phenotype, increase in surface expression of IL-1R8, diminishing activation mediated by toll-like receptor 4. Overall, IL-1R8 was identified as an important regulator of donor renal macrophage functions following ischemia-reperfusion injury, essential to guiding the phenotype and antigen-presenting role of these cells. It may, thus, be an intriguing pathway to investigate as regards to changing responses against autoantigens and alloantigens following a kidney transplant.