Dual inhibition of mTOR and calcineurin pathways mitigates missing self–induced NK cell–mediated microvascular rejection

S Sarah Hamada (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) J Jack Beadle (Centre for Inflammatory Disease, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London) A Alice Koenig (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) B Basile Sugranes (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) J John Ferdinand (Molecular Immunity Unit, Department of Medicine, University of Cambridge, MRC Laboratory of Molecular Biology) C Chien-Chia Chen (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) V Virginie Mathias (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) M Maeva Eloudzeri (Pathology Laboratory, Hôpital Necker-Enfants Malades, Assistance Publique-Hopitaux de Paris) T Thomas Barba (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) H Helena Paidassi C Carole Saison (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) V Valérie Dubois (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) E Emmanuel Morelon (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon) T Thierry Walzer A Antoine Marçais M Maud Rabeyrin (Pathology Laboratory, Hospices Civils de Lyon, Groupement Hospitalier Est) M Marion Rabant (Pathology Laboratory, Hôpital Necker-Enfants Malades, Assistance Publique-Hopitaux de Paris) P Patrick Bruneval M Maud Racapé (Université Paris Cité, INSERM U970, Paris Institute for Transplantation and Organ Regeneration) J Jean Paul Duong Van Huyen (Pathology Laboratory, Hôpital Necker-Enfants Malades, Assistance Publique-Hopitaux de Paris) M Menna R. Clatworthy C Candice Roufosse (Centre for Inflammatory Disease, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London) O Olivier Thaunat (Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon)

Abstract

The inability of graft endothelial cells to deliver HLA-I-dependent inhibitory signals to recipient natural killer (NK) cells (missing self, MS), drives donor-specific antibody-independent microvascular inflammation (MVI), leading to graft failure. This study aimed to elucidate the signaling pathways involved in MS-associated NK cell activation and explore therapeutic strategies. Analyses of kidney graft biopsies identified calcium signaling pathways and mTOR as a key regulator of MS-induced NK cell activation. Two experimental models were developed to mimic the pathological condition: in vitro cocultures of human NK cells with allogeneic microvascular endothelial cells and a murine heart transplantation model. These models showed that while calcineurin inhibitor (CNI) alone had a limited impact, combining CNI with mTOR inhibitors (mTORinh) synergistically reduced NK cell activation and endothelial damage. In a pilot clinical study involving 50 renal transplant recipients with MS-associated NK cell–mediated microvascular inflammation, patients who tolerated mTORinh introduced on top of CNI at diagnosis demonstrated reduced MVI lesions and improved graft survival compared to a historical cohort left on CNI and mycophenolate mofetil. This translational study identifies mTOR inhibition as a pivotal adjunct to CNI in mitigating MS-associated NK cell–mediated inflammation, potentially improving long-term graft outcomes.

Article Details

Volume / Issue Vol. 123, Issue 7
Published February 17, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (23)

S

Sarah Hamada

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

J

Jack Beadle

Centre for Inflammatory Disease, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London

A

Alice Koenig

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

B

Basile Sugranes

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

J

John Ferdinand

Molecular Immunity Unit, Department of Medicine, University of Cambridge, MRC Laboratory of Molecular Biology

C

Chien-Chia Chen

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

V

Virginie Mathias

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

M

Maeva Eloudzeri

Pathology Laboratory, Hôpital Necker-Enfants Malades, Assistance Publique-Hopitaux de Paris

T

Thomas Barba

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

H

Helena Paidassi

C

Carole Saison

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

V

Valérie Dubois

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

E

Emmanuel Morelon

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon

T

Thierry Walzer

A

Antoine Marçais

M

Maud Rabeyrin

Pathology Laboratory, Hospices Civils de Lyon, Groupement Hospitalier Est

M

Marion Rabant

Pathology Laboratory, Hôpital Necker-Enfants Malades, Assistance Publique-Hopitaux de Paris

P

Patrick Bruneval

M

Maud Racapé

Université Paris Cité, INSERM U970, Paris Institute for Transplantation and Organ Regeneration

J

Jean Paul Duong Van Huyen

Pathology Laboratory, Hôpital Necker-Enfants Malades, Assistance Publique-Hopitaux de Paris

M

Menna R. Clatworthy

C

Candice Roufosse

Centre for Inflammatory Disease, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London

O

Olivier Thaunat

Centre International de Recherche en Immunologie, Université de Lyon, INSERM U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon