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© Research
Publication : Nature communications

Missing self triggers NK cell-mediated chronic vascular rejection of solid organ transplants.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature communications - 25 Nov 2019

Koenig A, Chen CC, Marçais A, Barba T, Mathias V, Sicard A, Rabeyrin M, Racapé M, Duong-Van-Huyen JP, Bruneval P, Loupy A, Dussurgey S, Ducreux S, Meas-Yedid V, Olivo-Marin JC, Paidassi H, Guillemain R, Taupin JL, Callemeyn J, Morelon E, Nicoletti A, Charreau B, Dubois V, Naesens M, Walzer T, Defrance T, Thaunat O,

Link to Pubmed [PMID] – 31767837

Link to DOI – 10.1038/s41467-019-13113-5

Nat Commun 2019 11; 10(1): 5350

Current doctrine is that microvascular inflammation (MVI) triggered by a transplant -recipient antibody response against alloantigens (antibody-mediated rejection) is the main cause of graft failure. Here, we show that histological lesions are not mediated by antibodies in approximately half the participants in a cohort of 129 renal recipients with MVI on graft biopsy. Genetic analysis of these patients shows a higher prevalence of mismatches between donor HLA I and recipient inhibitory killer cell immunoglobulin-like receptors (KIRs). Human in vitro models and transplantation of β2-microglobulin-deficient hearts into wild-type mice demonstrates that the inability of graft endothelial cells to provide HLA I-mediated inhibitory signals to recipient circulating NK cells triggers their activation, which in turn promotes endothelial damage. Missing self-induced NK cell activation is mTORC1-dependent and the mTOR inhibitor rapamycin can prevent the development of this type of chronic vascular rejection.

https://pubmed.ncbi.nlm.nih.gov/31767837