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Extract Lung transplantation has evolved into a well-established therapeutic option for selected patients with end-stage lung disease, resulting in significantly improved quality of life and survival. However, despite improvements in surgical techniques and immunosuppressive therapies, prognosis remains less favourable compared to other solid organ transplants, due to several unique factors, such as persistent exposure to the external environment, risk of aspiration, ischaemia–reperfusion injury and abundant lymphoid tissue contained in the graft [1]. A range of alloimmune-dependent factors can contribute to chronic graft dysfunction, including acute cellular rejection, lymphocytic bronchiolitis, and human leukocyte antigen (HLA) mismatching. Additional risks arise from preformed or de novo anti-HLA antibodies, non-HLA antibodies, and antibodies directed against self-antigens, all of which can drive antibody-mediated rejection. Donor and recipient genetic variations, as well as non-adherence to immunosuppressive therapy, further compound the risk [2].
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Prasad et al. (2025) studied this question.
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