A B Cell‐Dependent Pathway Drives Chronic Lung Allograft Rejection After Ischemia‐Reperfusion Injury in Mice

摘要: Chronic lung allograft dysfunction (CLAD) limits long-term survival after transplant (LT). Ischemia-reperfusion injury (IRI) promotes chronic rejection (CR) and CLAD, but the underlying mechanisms are not well understood. To examine linking IRI to CR, a mouse orthotopic LT model using minor alloantigen strain mismatch (C57BL/10 [B10, H-2b ] → C57BL/6 [B6, ]) isograft controls (B6→B6) was used with antecedent minimal or prolonged graft storage. The latter resulted in subsequent airway parenchymal fibrosis storage allografts isografts. This pattern of CR associated formation B cell-rich tertiary lymphoid organs within grafts circulating autoantibodies. These processes were attenuated by cell depletion, despite preservation T content. Our observations suggest that may promote recruitment drives LT. have implications for leading CLAD