CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.

Humans Aorta Giant Cell Arteritis Immune Checkpoint Inhibitors Leukocytes, Mononuclear T-Lymphocytes, Regulatory CTLA-4 Antigen / metabolism
T-lymphocytes, regulatory giant cell arteritis humans immune checkpoint inhibitors vasculitis

Journal

Circulation research
ISSN: 1524-4571
Titre abrégé: Circ Res
Pays: United States
ID NLM: 0047103

Informations de publication

Date de publication:
04 08 2023
Historique:
medline: 7 8 2023
pubmed: 12 7 2023
entrez: 12 7 2023
Statut: ppublish

Résumé

Giant cell arteritis (GCA) causes severe inflammation of the aorta and its branches and is characterized by intense effector T-cell infiltration. The roles that immune checkpoints play in the pathogenesis of GCA are still unclear. Our aim was to study the immune checkpoint interplay in GCA. First, we used VigiBase, the World Health Organization international pharmacovigilance database, to evaluate the relationship between GCA occurrence and immune checkpoint inhibitors treatments. We then further dissected the role of immune checkpoint inhibitors in the pathogenesis of GCA, using immunohistochemistry, immunofluorescence, transcriptomics, and flow cytometry on peripheral blood mononuclear cells and aortic tissues of GCA patients and appropriated controls. Using VigiBase, we identified GCA as a significant immune-related adverse event associated with anti-CTLA-4 (cytotoxic T-lymphocyte-associated protein-4) but not anti-PD-1 (anti-programmed death-1) nor anti-PD-L1 (anti-programmed death-ligand 1) treatment. We further dissected a critical role for the CTLA-4 pathway in GCA by identification of the dysregulation of CTLA-4-derived gene pathways and proteins in CD4 We highlighted the instrumental role of CTLA-4 immune checkpoint in GCA, which provides a strong rationale for targeting this pathway.

Sections du résumé

BACKGROUND
Giant cell arteritis (GCA) causes severe inflammation of the aorta and its branches and is characterized by intense effector T-cell infiltration. The roles that immune checkpoints play in the pathogenesis of GCA are still unclear. Our aim was to study the immune checkpoint interplay in GCA.
METHODS
First, we used VigiBase, the World Health Organization international pharmacovigilance database, to evaluate the relationship between GCA occurrence and immune checkpoint inhibitors treatments. We then further dissected the role of immune checkpoint inhibitors in the pathogenesis of GCA, using immunohistochemistry, immunofluorescence, transcriptomics, and flow cytometry on peripheral blood mononuclear cells and aortic tissues of GCA patients and appropriated controls.
RESULTS
Using VigiBase, we identified GCA as a significant immune-related adverse event associated with anti-CTLA-4 (cytotoxic T-lymphocyte-associated protein-4) but not anti-PD-1 (anti-programmed death-1) nor anti-PD-L1 (anti-programmed death-ligand 1) treatment. We further dissected a critical role for the CTLA-4 pathway in GCA by identification of the dysregulation of CTLA-4-derived gene pathways and proteins in CD4
CONCLUSIONS
We highlighted the instrumental role of CTLA-4 immune checkpoint in GCA, which provides a strong rationale for targeting this pathway.

Identifiants

DOI: 10.1161/CIRCRESAHA.122.322330 PMID: 37435729
pubmed: 37435729
doi: 10.1161/CIRCRESAHA.122.322330
doi:

Substances chimiques

Immune Checkpoint Inhibitors 0
CTLA4 protein, human 0
CTLA-4 Antigen 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

298-312

Commentaires et corrections

Type : ErratumIn

Auteurs

Paul Régnier (P)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Biotherapy Unit (CIC-BTi), Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Groupe Hospitalier Pitié-Salpêtrière (P.R., A.L.J., A.M.-D., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
ORCID: 0000-0002-9713-1132

Alexandre Le Joncour (A)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Biotherapy Unit (CIC-BTi), Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Groupe Hospitalier Pitié-Salpêtrière (P.R., A.L.J., A.M.-D., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Département de Médecine Interne et Immunologie Clinique, Sorbonne Université, AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Paris, France (A.L.J., P.C., D.S.).
Centre National de Référence Maladies Autoimmunes Systémiques Rares, Centre National de Référence Maladies Autoinflammatoires et Amylose Inflammatoire, Inflammation-Immunopathology-Biotherapy Department (DMU 3iD), Paris, France (A.L.J., P.C., D.S.).

Anna Maciejewski-Duval (A)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Biotherapy Unit (CIC-BTi), Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Groupe Hospitalier Pitié-Salpêtrière (P.R., A.L.J., A.M.-D., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.

Guillaume Darrasse-Jèze (G)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Faculté de Médecine Paris Descartes (G.D.-J.), Université de Paris, France.
ORCID: 0000-0003-3069-8211

Charles Dolladille (C)

Normandie University, University of Caen Normandy, Centre Hospitalier Universitaire (CHU) de Caen Normandie, PICARO Cardio-Oncology Program, Department of Pharmacology, INSERM ANTICIPE U1086: Unité de Recherche Interdisciplinaire pour la Prévention et le Traitement des Cancers, Centre François Baclesse, France (C.D.).
ORCID: 0000-0003-0449-6261

Wouter C Meijers (WC)

Department of Cardiology, University Medical Center Groningen, University of Groningen, the Netherlands (W.C.M., J.-E.S.).

Lisa Bastarache (L)

Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN (L.B.).

Pierre Fouret (P)

Service d'anatomie et cytologie pathologiques, Groupe Hospitalier Pitié-Salpêtrière (P.F.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.

Patrick Bruneval (P)

Service d'anatomie pathologie, Hôpital Européen Georges Pompidou (P.B.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.

Floriane Arbaretaz (F)

Centre d'Histologie, d'Imagerie et de Cytométrie, Centre de Recherche des Cordeliers, Sorbonne Université, INSERM (F.A.), Université de Paris, France.
ORCID: 0000-0002-3972-5549

Célia Sayetta (C)

ICM Institut du Cerveau, CNRS UMR7225, INSERM U1127, Sorbonne Université, Hôpital de la Pitié-Salpêtrière, Paris, France (C.S.).

Ana Márquez (A)

Instituto de Parasitología y Biomedicina "López-Neyra," CSIC, PTS Granada, Spain (A.M.).
Systemic Autoimmune Disease Unit, Instituto de Investigación Biosanitaria de Granada, Spain (A.M.).

Michelle Rosenzwajg (M)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Biotherapy Unit (CIC-BTi), Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Groupe Hospitalier Pitié-Salpêtrière (P.R., A.L.J., A.M.-D., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
ORCID: 0000-0001-5312-6203

David Klatzmann (D)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Biotherapy Unit (CIC-BTi), Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Groupe Hospitalier Pitié-Salpêtrière (P.R., A.L.J., A.M.-D., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
ORCID: 0000-0002-0054-3422

Patrice Cacoub (P)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Biotherapy Unit (CIC-BTi), Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Groupe Hospitalier Pitié-Salpêtrière (P.R., A.L.J., A.M.-D., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Département de Médecine Interne et Immunologie Clinique, Sorbonne Université, AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Paris, France (A.L.J., P.C., D.S.).
Centre National de Référence Maladies Autoimmunes Systémiques Rares, Centre National de Référence Maladies Autoinflammatoires et Amylose Inflammatoire, Inflammation-Immunopathology-Biotherapy Department (DMU 3iD), Paris, France (A.L.J., P.C., D.S.).
ORCID: 0000-0002-6727-4992

Javid J Moslehi (JJ)

Section of Cardio-Oncology and Immunology, Division of Cardiology and the Cardiovascular Research Institute, University of California San Francisco (J.J.M.).
ORCID: 0000-0001-5443-4312

Joe-Elie Salem (JE)

Department of Pharmacology, INSERM, CIC-1901, UNICO-GRECO Cardiooncology Program, Sorbonne Université (J.-E.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Department of Cardiology, University Medical Center Groningen, University of Groningen, the Netherlands (W.C.M., J.-E.S.).
ORCID: 0000-0002-0331-3307

David Saadoun (D)

Immunology-Immunopathology-Immunotherapy (i3) Laboratory, INSERM UMR-S 959, Sorbonne Université, Paris, France (P.R., A.L.J., A.M.-D., G.D.-J., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Biotherapy Unit (CIC-BTi), Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Groupe Hospitalier Pitié-Salpêtrière (P.R., A.L.J., A.M.-D., M.R., D.K., P.C., D.S.), Assistance Publique-Hôpitaux de Paris (AP-HP), France.
Département de Médecine Interne et Immunologie Clinique, Sorbonne Université, AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Paris, France (A.L.J., P.C., D.S.).
Centre National de Référence Maladies Autoimmunes Systémiques Rares, Centre National de Référence Maladies Autoinflammatoires et Amylose Inflammatoire, Inflammation-Immunopathology-Biotherapy Department (DMU 3iD), Paris, France (A.L.J., P.C., D.S.).
ORCID: 0000-0003-3628-9996

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.
questionsmedicales.fr › Système cardiovasculaire › Vaisseaux sanguins › Artères › Aorte › CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.
questionsmedicales.fr › Maladies du système immunitaire › Maladies auto-immunes › Maladies auto-immunes du système nerveux › Vascularite du système nerveux central › Artérite à cellules géantes › CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.
questionsmedicales.fr › Actions chimiques et utilisations › Actions pharmacologiques › Utilisations thérapeutiques › Antinéoplasiques › Antinéoplasiques immunologiques › Inhibiteurs de points de contrôle immunitaires › CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.
questionsmedicales.fr › Systèmes sanguin et immunitaire › Système immunitaire › Leucocytes › Agranulocytes › CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.
questionsmedicales.fr › Systèmes sanguin et immunitaire › Système immunitaire › Leucocytes › Agranulocytes › Lymphocytes › Lymphocytes T › Sous-populations de lymphocytes T › Lymphocytes T régulateurs › CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.
questionsmedicales.fr › Facteurs biologiques › Marqueurs biologiques › Antigènes de différenciation › Antigènes de différenciation des lymphocytes T › Antigène CTLA-4 › CTLA-4 Pathway Is Instrumental in Giant Cell Arteritis.