Key result
Innate immune stimuli contribute to CLAD and late allograft fibrosis after lung transplantation.
Why the study?
Long-term survival after lung transplantation is limited by chronic lung allograft dysfunction, whose underlying mechanisms involving innate immunity are not fully elucidated and lack effective prevention or treatment.
This review highlights the fundamental role of innate immune stimuli in the development of chronic lung allograft dysfunction, offering potential new mechanistic insights for a condition that currently lacks effective treatments.
May support innate immune-targeted therapies in lung transplant recipients; leaves open whether modulation improves clinical outcomes.
Long-term survival after lung transplantation remains suboptimal due to chronic lung allograft dysfunction (CLAD), a progressive scarring process affecting the graft. Although anti-donor alloimmunity is central to the pathogenesis of CLAD, its underlying mechanisms are not fully elucidated and it is neither preventable nor treatable using currently available immunosuppression. Recent evidence has shown that innate immune stimuli are fundamental to the development of CLAD. Here, we examine long-standing assumptions and new concepts linking innate immune activation to late lung allograft fibrosis.
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Kawashima et al. (2020) conducted a review in Chronic lung allograft dysfunction (CLAD) after lung transplantation. Innate immune activation was evaluated on Late lung allograft fibrosis / CLAD. Innate immune stimuli are fundamental to the development of chronic lung allograft dysfunction and late lung allograft fibrosis after lung transplantation.
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