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

Hrishikesh S Kulkarni1,2, Laneshia K Tague1, Daniel R Calabrese3,4

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|November 11, 2025
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Summary
This summary is machine-generated.

Genetic predisposition to complement activation, specifically the C3 R102G polymorphism, is linked to worse chronic lung allograft dysfunction (CLAD)-free survival after lung transplantation (LTx) due to increased antibody responses.

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Area of Science:

  • Immunology
  • Transplantation Biology
  • Genetics

Background:

  • Chronic lung allograft dysfunction (CLAD) is the main cause of death after lung transplantation (LTx).
  • The complement system plays a crucial role in immune responses and is activated early post-LTx.
  • Understanding CLAD pathobiology is essential for improving LTx outcomes.

Purpose of the Study:

  • To investigate the association between a genetic predisposition to enhanced complement activation and CLAD-free survival in LTx recipients.
  • To explore the role of the C3 R102G polymorphism in CLAD development and alloimmunity.
  • To elucidate the mechanisms linking complement dysregulation to humoral immune responses in LTx.

Main Methods:

  • Analysis of a functional C3 polymorphism (C3 R102G) in two independent LTx recipient cohorts.
  • Association studies correlating C3 R102G genotype with CLAD-free survival and donor-specific antibodies (DSAs).
  • Utilized a mouse orthotopic LTx model to study the impact of impaired complement regulation on CLAD pathology.

Main Results:

  • The C3 R102G polymorphism, present in over one-third of LTx recipients, was associated with significantly worse CLAD-free survival.
  • This association was particularly pronounced in recipients who developed DSAs.
  • In the mouse model, impaired complement regulation led to B cell-dependent CLAD and increased DSA levels.

Conclusions:

  • Genetic predisposition to complement activation, via C3 R102G, contributes to poorer CLAD-free survival after LTx.
  • Enhanced complement activation promotes a detrimental humoral immune response, characterized by increased DSAs.
  • Targeting complement dysregulation may represent a therapeutic strategy to improve LTx outcomes.