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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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Genetic predisposition to complement activation is linked to worse outcomes after lung transplantation (LTx). This genetic factor promotes B cell activation, increasing the risk of chronic lung allograft dysfunction (CLAD).

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Area of Science:

  • Immunology
  • Transplantation Science
  • Genetics

Background:

  • Chronic lung allograft dysfunction (CLAD) is a major cause of mortality following lung transplantation (LTx).
  • The complement system plays a crucial role in innate and adaptive immunity, becoming active early after LTx.
  • Understanding the genetic factors influencing complement activation is vital for improving LTx outcomes.

Purpose of the Study:

  • To investigate the association between a specific genetic polymorphism in complement component 3 (C3R102G) and CLAD-free survival in LTx recipients.
  • To explore the role of impaired complement regulation in adaptive alloimmunity and CLAD development.
  • To determine the impact of complement activation on B cell populations and donor-specific antibody (DSA) levels.

Main Methods:

  • Analysis of a functional C3 polymorphism (C3R102G) in two independent LTx recipient cohorts.
  • Assessment of CLAD-free survival in relation to C3R102G status, particularly in DSA-positive recipients.
  • Utilizing a mouse orthotopic lung transplantation model to study the effects of impaired complement regulation on graft pathology and immune cell infiltration.

Main Results:

  • The C3R102G polymorphism, present in over one-third of LTx recipients, was associated with significantly worse CLAD-free survival.
  • This association was more pronounced in recipients who developed donor-specific antibodies (DSA).
  • In a mouse model, impaired complement regulation led to more severe airway lesions and increased intragraft accumulation of memory B cells and antibody-secreting cells, correlating with higher DSA levels.

Conclusions:

  • A genetic predisposition to enhanced complement activation, via the C3R102G polymorphism, is linked to poorer CLAD-free survival after lung transplantation.
  • Impaired complement regulation promotes B cell activation and antibody production, contributing to the development of CLAD.
  • Targeting complement pathways may offer a therapeutic strategy to mitigate CLAD and improve long-term lung allograft survival.