Abstract
Lung transplant patients have the lowest long-term survival rates compared to other solid organ transplants. The complications after lung transplantation such as primary graft dysfunction (PGD) and ultimately chronic lung allograft dysfunction (CLAD) are the main reasons for this limited survival. In recent years, lung-specific autoantibodies that recognize non-HLA antigens have been hypothesized to contribute to graft injury and have been correlated with PGD, CLAD, and survival. Mounting evidence suggests that autoantibodies can develop during pulmonary disease progression before lung transplant, termed pre-existing autoantibodies, and may participate in allograft injury after transplantation. In this review, we summarize what is known about pulmonary disease autoantibodies, the relationship between pre-existing autoantibodies and lung transplantation, and potential mechanisms through which pre-existing autoantibodies contribute to graft injury and rejection.
Highlights
Lung transplantation (LTx) is the only viable option for many chronic end-stage pulmonary diseases (CPD)
Chronic obstructive pulmonary disease (COPD) is a group of progressive pulmonary disorders characterized by chronic pulmonary inflammation and damage to small airways and alveolar airspace that results in airflow limitation
We discovered that all four IgG anti-elastin pre-existing autoantibodies are elevated in cigarette smoke (CS) exposed mice compared to controls
Summary
Lung transplantation (LTx) is the only viable option for many chronic end-stage pulmonary diseases (CPD). Following IRI, activation of innate and adaptive immune response drives targeted graft damage This damage manifests as post-Tx complications such as PGD, acute rejection, and CLAD, all of which predispose to increased risk of mortality. The generally accepted model of immune-mediated graft damage proposes a feed-forward mechanism starting with donor graft injury, IRI-mediated immune activation and graft damage, thereby promoting subsequent adaptive immune activation and T cell specific graft damage. This model does not take into account the recipients’ lung specific pre-Tx immune system. We highlight recent advances in the association between autoantibodies and COPD and ILD patients (Table 1)
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