Antibody-mediated allograft rejection is associated with an increase in peripheral differentiated CD28-CD8+ T cells - Analyses of a cohort of 1032 kidney transplant recipients.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Sep 2022
Historique:
received: 26 07 2021
revised: 24 06 2022
accepted: 01 08 2022
pubmed: 22 8 2022
medline: 21 9 2022
entrez: 21 8 2022
Statut: ppublish

Résumé

CD28-CD8+ T cells represent a differentiated CD8+ T cell subset that is found to be increased in various conditions associated with chronic antigenic stimulation such as aging, chronic viral infections, autoimmune diseases, cancers, and allotransplantation. Using multivariate models, we analyzed a large cohort of 1032 kidney transplant patients in whom 1495 kidney graft biopsies were performed concomitant with a peripheral blood leukocyte phenotyping by flow cytometry. We investigated the association between the level of CD28-CD8+ T cells in the blood and the diagnosis of graft rejection according to the recent Banff classification of renal allograft pathology. We found that antibody-mediated rejection (ABMR) was associated with a significant increase in the percentage as well as the absolute number of CD28-CD8+ T cells in the peripheral blood of kidney transplant patients at the time of biopsy. The confounder-adjusted mean difference of log percentage and log absolute value between the ABMR group and the normal/subnormal histology group were 0.29 (p=0.0004) and 0.38 (p=0.0004), respectively. Moreover, we showed that CD28-CD8+ T cells from the patients diagnosed with ABMR responded more rigorously to TCR and FcγRIIIA (CD16) engagement compared to their CD28+ counterparts as evidenced by an increase in the expression of IFNγ, TNFα, and CD107a. Collectively, our data suggest that differentiated CD28-CD8+ T cells, with increased frequency, number, and function, may participate in the pathobiology of ABMR. Further studies are warranted to clarify the immunological role of this T cell subset in kidney graft rejection. Agence nationale de la recherche (France).

Sections du résumé

BACKGROUND BACKGROUND
CD28-CD8+ T cells represent a differentiated CD8+ T cell subset that is found to be increased in various conditions associated with chronic antigenic stimulation such as aging, chronic viral infections, autoimmune diseases, cancers, and allotransplantation.
METHODS METHODS
Using multivariate models, we analyzed a large cohort of 1032 kidney transplant patients in whom 1495 kidney graft biopsies were performed concomitant with a peripheral blood leukocyte phenotyping by flow cytometry. We investigated the association between the level of CD28-CD8+ T cells in the blood and the diagnosis of graft rejection according to the recent Banff classification of renal allograft pathology.
FINDINGS RESULTS
We found that antibody-mediated rejection (ABMR) was associated with a significant increase in the percentage as well as the absolute number of CD28-CD8+ T cells in the peripheral blood of kidney transplant patients at the time of biopsy. The confounder-adjusted mean difference of log percentage and log absolute value between the ABMR group and the normal/subnormal histology group were 0.29 (p=0.0004) and 0.38 (p=0.0004), respectively. Moreover, we showed that CD28-CD8+ T cells from the patients diagnosed with ABMR responded more rigorously to TCR and FcγRIIIA (CD16) engagement compared to their CD28+ counterparts as evidenced by an increase in the expression of IFNγ, TNFα, and CD107a.
INTERPRETATION CONCLUSIONS
Collectively, our data suggest that differentiated CD28-CD8+ T cells, with increased frequency, number, and function, may participate in the pathobiology of ABMR. Further studies are warranted to clarify the immunological role of this T cell subset in kidney graft rejection.
FUNDING BACKGROUND
Agence nationale de la recherche (France).

Identifiants

pubmed: 35988467
pii: S2352-3964(22)00408-X
doi: 10.1016/j.ebiom.2022.104226
pmc: PMC9420477
pii:
doi:

Substances chimiques

Antibodies 0
CD28 Antigens 0
Receptors, Antigen, T-Cell 0
Tumor Necrosis Factor-alpha 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

104226

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests All authors declared no conflict of interest.

Auteurs

Hoa Le Mai (HL)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France.

Nicolas Degauque (N)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France.

Sabine Le Bot (S)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France; Service de Néphrologie et Immunologie Clinique, CHU Nantes, Nantes, France.

Marie Rimbert (M)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France; Laboratoire d'Immunologie, Centre d'ImmunoMonitorage Nantes-Atlantique (CIMNA), CHU Nantes, Nantes, France.

Karine Renaudin (K)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France; Service d'Anatomie et Cytologie Pathologiques, CHU Nantes, Nantes, France.

Richard Danger (R)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France.

Florent Le Borgne (F)

IDBC-A2COM, Nantes, France; INSERM UMR 1246 - SPHERE, Nantes, France.

Clarisse Kerleau (C)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France.

Gaelle Tilly (G)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France.

Anaïs Vivet (A)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France.

Florent Delbos (F)

Etablissement Français du Sang (EFS), Nantes, France.

Alexandre Walencik (A)

Etablissement Français du Sang (EFS), Nantes, France.

Magali Giral (M)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France; Service de Néphrologie et Immunologie Clinique, CHU Nantes, Nantes, France; Fondation Centaure (RTRS), Nantes, France. Electronic address: magali.giral@chu-nantes.fr.

Sophie Brouard (S)

CHU Nantes, Nantes Université, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, F-44000 Nantes, France; Fondation Centaure (RTRS), Nantes, France. Electronic address: sophie.brouard@univ-nantes.fr.

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