Key result
Autoimmunity, driven by autoantibodies to collagen type V and K-alpha1 tubulin and mediated by IL-17, plays a key role in the development of obliterative bronchiolitis after lung transplantation.
Autoimmunity, driven by IL-17 and autoantibodies to self-antigens like collagen type V, is a major contributor to chronic lung allograft rejection, offering potential new therapeutic targets.
May highlight IL-17 pathways as therapeutic targets after lung transplant; leaves open prospective trials before practice change.
First performed in the 1960s with long-term successes achieved in the 1980s, lung transplantation remains the only definitive treatment option for end-stage lung disease. Chronic lung rejection, pathologically classified as obliterative bronchiolitis (OB) with its clinical correlate referred to as bronchiolitis obliterans syndrome, is the limiting factor than keeps 5-yr survival rates for lung transplant significantly worse than for other solid organ transplants. Initially, OB was largely attributed to immune responses to donor antigens, alloimmunity. However, more recent work has demonstrated the role of autoimmunity in the process of lung transplant rejection. IL-17 and autoantigens such as collagen type V and K-α1 tubulin have been implicated in the development of chronic rejection. Ultimately, this translational review discusses the role that autoimmunity plays in the development of OB and lung transplant rejection and then discusses options for therapeutic intervention.
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Weber et al. (2012) conducted a review in Obliterative bronchiolitis after lung transplantation. Autoimmunity was evaluated. Autoimmunity, driven by autoantibodies to collagen type V and K-alpha1 tubulin and mediated by IL-17, plays a key role in the development of obliterative bronchiolitis after lung transplantation.
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