Primary graft dysfunction grade 3 following pediatric lung transplantation is associated with chronic lung allograft dysfunction

Wong, Wai; Johnson, Brandy N.; Cheng, Pi Chun; Josephson, Maureen; Maeda, Katsuhide; Berg, Robert A.; Kawut, Steven M.; Harhay, Michael O.; Goldfarb, Samuel; Yehya, Nadir; Himebauch, Adam S.

doi:10.1016/j.healun.2022.12.014

Cited by 3 publications

(1 citation statement)

References 36 publications

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“…Furthermore, PGD was associated with an increased mortality rate at one year [OR 1.7 (95% CI 1.2, 2.3), p = .0001] ( 33 ). PGD has also been linked with a higher risk of CLAD and poorer long-term outcomes ( 34 , 35 ).…”

Section: Pre-existing Lra Development and Their Role In Pgdmentioning

confidence: 99%

The role of lung-restricted autoantibodies in the development of primary and chronic graft dysfunction

Yang,

Lecuona,

et al. 2023

Front. Transplant.

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Lung transplantation is a life-saving treatment for both chronic end-stage lung diseases and acute respiratory distress syndrome, including those caused by infectious agents like COVID-19. Despite its increasing utilization, outcomes post-lung transplantation are worse than other solid organ transplants. Primary graft dysfunction (PGD)—a condition affecting more than half of the recipients post-transplantation—is the chief risk factor for post-operative mortality, transplant-associated multi-organ dysfunction, and long-term graft loss due to chronic rejection. While donor-specific antibodies targeting allogenic human leukocyte antigens have been linked to transplant rejection, the role of recipient's pre-existing immunoglobulin G autoantibodies against lung-restricted self-antigens (LRA), like collagen type V and k-alpha1 tubulin, is less understood in the context of lung transplantation. Recent studies have found an increased risk of PGD development in lung transplant recipients with LRA. This review will synthesize past and ongoing research—utilizing both mouse models and human subjects—aimed at unraveling the mechanisms by which LRA heightens the risk of PGD. Furthermore, it will explore prospective approaches designed to mitigate the impact of LRA on lung transplant patients.

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Section: Pre-existing Lra Development and Their Role In Pgdmentioning

confidence: 99%

The role of lung-restricted autoantibodies in the development of primary and chronic graft dysfunction

Yang,

Lecuona,

et al. 2023

Front. Transplant.

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Fibrotic progression from acute cellular rejection is dependent on secondary lymphoid organs in a mouse model of chronic lung allograft dysfunction

Mineura,

Tanaka,

Goda

et al. 2024

American Journal of Transplantation

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Update on the immunological mechanisms of primary graft dysfunction and chronic lung allograft dysfunction

Jeong,

Gelman,

Chong

2024

Current Opinion in Organ Transplantation

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Purpose of review Primary graft dysfunction (PGD) and chronic lung allograft dysfunction (CLAD) are the leading causes of graft loss in lung transplant recipients. The development of mouse lung transplant models has allowed for the genetic dissection of cellular and molecular pathways that prevent graft survival. This review provides an overview into recent mechanistic insights into PGD and CLAD. Recent findings Mouse orthotopic lung transplant models and investigations of human lung transplant recipeints have revealed new molecular and cellular targets that promote PGD and CLAD. Donor and recipient-derived innate immune cells promote PGD and CLAD. PGD is driven by communication between classical monocytes and tissue-resident nonclassical monocytes activating alveolar macrophages to release chemokines that recruit neutrophils. Products of cell damage trigger neutrophil NET release, which together with NK cells, antibodies and complement, that further promote PGD. The development of CLAD involves circuits that activate B cells, CD8+ T cells, classical monocytes, and eosinophils. Summary Effective targeted management of PGD and CLAD in lung transplant recipient to improve their long-term outcome remains a critical unmet need. Current mechanistic studies and therapeutic studies in mouse models and humans identify new possibilities for prevention and treatment.

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Primary graft dysfunction grade 3 following pediatric lung transplantation is associated with chronic lung allograft dysfunction

Cited by 3 publications

References 36 publications

The role of lung-restricted autoantibodies in the development of primary and chronic graft dysfunction

The role of lung-restricted autoantibodies in the development of primary and chronic graft dysfunction

Fibrotic progression from acute cellular rejection is dependent on secondary lymphoid organs in a mouse model of chronic lung allograft dysfunction

Update on the immunological mechanisms of primary graft dysfunction and chronic lung allograft dysfunction

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