Radiomic analysis of liver grafts from brain-dead donors can predict early allograft dysfunction following transplantation: a proof-of-concept study

Robin, Fabien; Khene, Z.; Livin, Marie; Sumner, C.; Houssel‐Debry, Pauline; Sulpice, Laurent; Boudjéma, Karim

doi:10.1016/j.hpb.2022.03.009

Cited by 1 publication

(2 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our cohort, donor BMI, donor graft weight, liver fatty change and CIT were associated with the incidence of EAD after transplantation. These have been frequently reported as risk factors for EAD 15–17 . Among them, only CIT was found to be related to the NK cell shift.…”

Section: Discussionmentioning

confidence: 96%

See 1 more Smart Citation

Dynamic immune cell profiling identified natural killer cell shift as the key event in early allograft dysfunction after liver transplantation

Lu,

Yang,

Pan

et al. 2023

Cell Proliferation

View full text Add to dashboard Cite

Early allograft dysfunction (EAD) is a life‐threatening and fast‐developing complication after liver transplantation. The underlying mechanism needs to be better understood, and there has yet to be an efficient therapeutic target. This study retrospectively reviewed 109 patients undergoing liver transplantation, with dynamic profiling of CD3/4/8/16/19/45/56 on the peripheral immune cells (before transplant and 2–4 days after). Altogether, 35 out of the 109 patients developed EAD after liver transplantation. We observed a significant decrease in the natural killer cell proportion (NK cell shift, p = 0.008). The NK cell shift was linearly correlated with cold ischemic time (p = 0.016) and was potentially related to the recipients' outcomes. In mouse models, ischemic/reperfusion (I/R) treatments induced the recruitment of NK cells from peripheral blood into liver tissues. NK cell depletion blocked a series of immune cascades (including CD8+ CD127+ T cells) and inhibited hepatocyte injury effectively in I/R and liver transplantation models. We further found that I/R treatment increased hepatic expression of the ligands for natural killer group 2 member D (NKG2D), a primary activating cell surface receptor in NK cells. Blockade of NKG2D showed a similar protective effect against I/R injury, indicating its role in NK cell activation and the subsequent immunological injury. Our findings built a bridge for the translation from innate immune response to EAD at the bedside. Peripheral NK cell shift is associated with the incidence of EAD after liver transplantation. NKG2D‐mediated NK cell activation is a potential therapeutic target.

show abstract

Section: Discussionmentioning

confidence: 96%

“…These have been frequently reported as risk factors for EAD. 15 , 16 , 17 Among them, only CIT was found to be related to the NK cell shift. Prolonged CIT is one of the critical elements in transplanted organ I/R injury.…”

Section: Discussionmentioning

confidence: 99%