Impaired complement regulation drives chronic lung allograft dysfunction after lung transplantation.

ABSTRACT: A greater understanding of chronic lung allograft dysfunction (CLAD) pathobiology, the primary cause of mortality after lung transplantation (LTx), is needed to improve outcomes. The complement system links innate to adaptive immune responses and is activated early post-lung transplantation to form the C3 convertase, a critical enzyme that cleaves the central complement component C3. We hypothesized that LTx recipients with a genetic predisposition to enhanced complement activation have worse CLAD-free survival mediated through increased adaptive alloimmunity. We interrogated a known functional C3 polymorphism (C3R102G) that increases complement activation through impaired C3 convertase inactivation in two independent LTx recipient cohorts. C3R102G, identified in at least one out of three

SUBMITTER: Kulkarni HS 

PROVIDER: S-EPMC12721912 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature