Autoantibodies in lung transplantation

Abstract

Chronic lung allograft dysfunction (CLAD) comprises both bronchiolitis obliterans syndrome and restrictive allograft syndrome as subtypes. After lung transplantation, CLAD remains a major limitation for long-term survival, and lung transplant recipients therefore have poorer outcomes compared with recipients of other solid organ transplants. Although the number of lung transplants continues to increase globally, the field demands detailed understanding of immunoregulatory mechanisms and more effective individualized therapies to combat CLAD. Emerging evidence suggests that CLAD is multifactorial and involves a complex, delicate interplay of multiple factors, including perioperative donor characteristics, inflammation induced immediately following transplant, post-transplant infection and interplay between allo- and autoimmunity directed to donor antigens. Recently, identification of stress-induced exosome release from the transplanted organ has emerged as an underlying mechanism in the development of chronic rejection and promises to prompt novel strategies for future therapeutic interventions. In this review, we will discuss recent studies and ongoing research into the mechanisms for the development of CLAD, with emphasis on immune responses to lung-associated self-antigens-that is, autoimmunity.

Keywords: K-alpha 1 tubulin; alloimmunity; autoimmunity; chronic lung allograft dysfunction; collagen V; exosomes.