ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2021
A decline in club cell secretory proteins in lung transplantation is associated with release of natural killer cells exosomes leading to chronic rejection.
Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Noninvasive biomarkers for the detection of GERD-induced pulmonary injury.Surgical endoscopy · 2024Article
- The exosome: a review of current therapeutic roles and capabilities in human reproduction.Drug delivery and translational research · 2023Review
- Extracellular Vesicles Mediate Immune Responses to Tissue-Associated Self-Antigens: Role in Solid Organ Transplantations.Frontiers in immunology · 2022Review
- Assessment of patient-to-patient and intra-individual human abdominal skin immune cell variability.Archives of medical science : AMS · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIn human lung transplant recipients, a decline in club cell secretory protein (CCSP) in bronchoalveolar lavage fluid has been associated with chronic lung allograft dysfunction (CLAD) as well as the induction of exosomes and immune responses that lead to CLAD. However, the mechanisms by which CCSP decline contributes to CLAD remain unknown.
methodsTo define the mechanisms leading to CCSP decline and chronic rejection, we employed two mouse models: 1) chronic rejection after orthotopic single lung transplantation and 2) anti-major histocompatibility complex (MHC) class I-induced obliterative airway disease.
resultsIn the chronic rejection mouse model, we detected circulating exosomes with donor MHC (H2
conclusionsInduction of exosomes led to immune responses to donor MHC and lung self-antigens, resulting in CCSP decline, leading to NK cell infiltration and release of exosomes from NK cells. These results suggest a novel role for exosomes derived from NK cells in the pathogenesis of chronic lung allograft rejection.
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