Azathioprine therapy induces selective NK cell depletion and IFN-γ deficiency predisposing to herpesvirus reactivation.

Azathioprine IFN-γ NK cells adverse effects full-spectrum cytometry herpesvirus immune signature immunosuppression mass cytometry myasthenia gravis side effects

Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
01 2023
Historique:
received: 04 04 2022
revised: 17 08 2022
accepted: 01 09 2022
pubmed: 20 9 2022
medline: 11 1 2023
entrez: 19 9 2022
Statut: ppublish

Résumé

Azathioprine is a widely prescribed drug for patients with chronic inflammatory diseases such as myasthenia gravis or organ transplant recipients. Azathioprine exerts immunosuppressive effects by inhibiting intracellular purine synthesis and reducing the numbers of circulating B and T lymphocytes. Case reports indicate increased risk for serious infections that can occur despite regular measurements of lymphocyte counts during azathioprine therapy. We sought to comprehensively investigate therapy-associated patient risks and the underlying immune dysfunction of azathioprine use. Peripheral blood leukocytes were analyzed using single-cell mass and spectral flow cytometry to detect specific effects of azathioprine use on the systemic immune signature. Therapy-associated clinical features were analyzed in 2 independent cohorts of myasthenia gravis patients. Azathioprine therapy selectively induced pronounced CD56 Our study highlights the risk of development of adverse events during azathioprine therapy and suggests that natural killer cell monitoring could be valuable in clinical practice.

Sections du résumé

BACKGROUND
Azathioprine is a widely prescribed drug for patients with chronic inflammatory diseases such as myasthenia gravis or organ transplant recipients. Azathioprine exerts immunosuppressive effects by inhibiting intracellular purine synthesis and reducing the numbers of circulating B and T lymphocytes. Case reports indicate increased risk for serious infections that can occur despite regular measurements of lymphocyte counts during azathioprine therapy.
OBJECTIVE
We sought to comprehensively investigate therapy-associated patient risks and the underlying immune dysfunction of azathioprine use.
METHODS
Peripheral blood leukocytes were analyzed using single-cell mass and spectral flow cytometry to detect specific effects of azathioprine use on the systemic immune signature. Therapy-associated clinical features were analyzed in 2 independent cohorts of myasthenia gravis patients.
RESULTS
Azathioprine therapy selectively induced pronounced CD56
CONCLUSION
Our study highlights the risk of development of adverse events during azathioprine therapy and suggests that natural killer cell monitoring could be valuable in clinical practice.

Identifiants

pubmed: 36122787
pii: S0091-6749(22)01187-3
doi: 10.1016/j.jaci.2022.09.010
pii:
doi:

Substances chimiques

Azathioprine MRK240IY2L
Interferon-gamma 82115-62-6

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

280-286.e2

Informations de copyright

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

Auteurs

Florian Ingelfinger (F)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland; Department of Neurology, University Hospital Zurich, Zurich, Switzerland.

Colin Sparano (C)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

David Bamert (D)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

David Reyes-Leiva (D)

Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; Department of Medicine, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III, Madrid, Spain.

Aakriti Sethi (A)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Lukas Rindlisbacher (L)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Pascale Zwicky (P)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Stefanie Kreutmair (S)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Corinne C Widmer (CC)

Department of Medical Oncology and Hematology, University Hospital Zurich and the University of Zurich, Zurich, Switzerland.

Sarah Mundt (S)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Elena Cortés-Vicente (E)

Neuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; Department of Medicine, Universitat Autònoma de Barcelona, Spain; Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III, Madrid, Spain.

Sonia Tugues (S)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Burkhard Becher (B)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland. Electronic address: becher@immunology.uzh.ch.

Bettina Schreiner (B)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland; Department of Neurology, University Hospital Zurich, Zurich, Switzerland. Electronic address: bettina.schreiner@uzh.ch.

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Classifications MeSH