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1. Human monocyte-derived suppressive cells (HuMoSC) for cell therapy in giant cell arteritis

Author

Maxime Samson, Coraline Genet, Marc Corbera-Bellalta, Hélène Greigert, Georgina Espígol-Frigolé, Claire Gérard, Claudie Cladière, Roser Alba-Rovira, Marion Ciudad, Pierre-Henry Gabrielle, Catherine Creuzot-Garcher, Georges Tarris, Laurent Martin, Philippe Saas, Sylvain Audia, Bernard Bonnotte, and Maria C. Cid

Subjects
suppressive cells, giant cell arteritis, treatment, cellular therapy, vascular remodeling, Immunologic diseases. Allergy, RC581-607
Abstract

IntroductionThe pathogenesis of Giant Cell Arteritis (GCA) relies on vascular inflammation and vascular remodeling, the latter being poorly controlled by current treatments.MethodsThis study aimed to evaluate the effect of a novel cell therapy, Human Monocyte-derived Suppressor Cells (HuMoSC), on inflammation and vascular remodeling to improve GCA treatment. Fragments of temporal arteries (TAs) from GCA patients were cultured alone or in the presence of HuMoSCs or their supernatant. After five days, mRNA expression was measured in the TAs and proteins were measured in culture supernatant. The proliferation and migration capacity of vascular smooth muscle cells (VSMCs) were also analyzed with or without HuMoSC supernatant. ResultsTranscripts of genes implicated in vascular inflammation (CCL2, CCR2, CXCR3, HLADR), vascular remodeling (PDGF, PDGFR), angiogenesis (VEGF) and extracellular matrix composition (COL1A1, COL3A1 and FN1) were decreased in arteries treated with HuMoSCs or their supernatant. Likewise, concentrations of collagen-1 and VEGF were lower in the supernatants of TAs cultivated with HuMoSCs. In the presence of PDGF, the proliferation and migration of VSMCs were both decreased after treatment with HuMoSC supernatant. Study of the PDGF pathway suggests that HuMoSCs act through inhibition of mTOR activity. Finally, we show that HuMoSCs could be recruited in the arterial wall through the implication of CCR5 and its ligands.ConclusionAltogether, our results suggest that HuMoSCs or their supernatant could be useful to decrease vascular in flammation and remodeling in GCA, the latter being an unmet need in GCA treatment.

Published
2023
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2. Improvement of Treg immune response after treatment with tocilizumab in giant cell arteritis

Author

Maxime Samson, Hélène Greigert, Marion Ciudad, Claire Gerard, Thibault Ghesquière, Malika Trad, Marc Corbera‐Bellalta, Coraline Genet, Sethi Ouandji, Claudie Cladière, Marine Thebault, Kim Heang Ly, Eric Liozon, François Maurier, Boris Bienvenu, Benjamin Terrier, Loïc Guillevin, Pierre Charles, Valérie Quipourt, Hervé Devilliers, Pierre‐Henry Gabrielle, Catherine Creuzot‐Garcher, Georges Tarris, Laurent Martin, Philippe Saas, Sylvain Audia, Maria Cinta Cid, and Bernard Bonnotte

Subjects
giant cell arteritis, interleukin‐6, tocilizumab, Treg, Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Objectives To study the percentage, suppressive function and plasticity of Treg in giant cell arteritis (GCA), and the effects of glucocorticoids and tocilizumab. Methods Blood samples were obtained from 40 controls and 43 GCA patients at baseline and after treatment with glucocorticoids + IV tocilizumab (n = 20) or glucocorticoids (n = 23). Treg percentage and phenotype were assessed by flow cytometry. Suppressive function of Treg was assessed by measuring their ability to inhibit effector T‐cell (Teff) proliferation and polarisation into Th1 and Th17 cells. Results Treg (CD4+CD25highFoxP3+) frequency in total CD4+ T cells was decreased in active GCA patients when compared to controls (2.5% vs. 4.7%, P

Published
2021
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3. Myocardial infarction during giant cell arteritis: A cohort study

Author

Tibor Ponnelle, Sylvain Audia, Bernard Bonnotte, G. Muller, Alain Putot, Georges Tarris, André Ramon, Maxime Samson, Yves Cottin, Eric Steinmetz, Marianne Zeller, Nicolas Falvo, Béatrice Terriat, Maud Maza, Laurent Martin, Hélène Greigert, Catherine Creuzot-Garcher, Louis Arnould, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Cypath [Dijon], Cypath : siège social [Villeurbanne], and The University Hospital of Dijon, the Association de Cardiologie de Bourgogne, and by grants from the Agence Regionale de Sante (ARS) de Bourgogne Franche-Comte, and from the Regional Council of Bourgogne Franche-Comte.

Subjects
medicine.medical_specialty, Population, Coronary Artery Disease, 030204 cardiovascular system & hematology, Cohort Studies, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, immune system diseases, Prednisone, Internal medicine, Internal Medicine, medicine, Humans, cardiovascular diseases, 030212 general & internal medicine, Myocardial infarction, skin and connective tissue diseases, education, education.field_of_study, population study, giant cell arteritis, business.industry, medicine.disease, 3. Good health, Giant cell arteritis, myocardial infarction, Cohort, cardiovascular system, Cardiology, Population study, France, business, medicine.drug, Cohort study
Abstract

International audience; BACKGROUND: Cardiovascular risk is increased in giant cell arteritis (GCA). We aimed to characterize myocardial infarction (MI) in a GCA cohort, and to compare the GCA and non-GCA population affected by MI. METHODS: In patients with a biopsy-proven diagnosis of GCA between 1 January 2001 and 31 December 2016 in Côte D'Or (France), we identified patients with MI by crossing data from the territorial myocardial infarction registry (Observatoire des Infarctus de Côte d'Or) database. Five controls (non-GCA + MI) were paired with one case (GCA + MI) after matching for age, sex, cardiovascular risk factors and prior cardiovascular disease. MI were characterized as type 1 MI (T1MI), resulting from thrombus formation due to atherothrombotic disease, or type 2 MI (T2MI), due to a myocardial supply/demand mismatch. GCA-related MI was defined as MI occurring within 3 months of a GCA flare (before or after). RESULTS: Among 251 biopsy-proven GCA patients, 13 MI cases were identified and paired with 65 controls. MI was GCA-related in 6/13 cases, accounting for 2.4% (6/251) of our cohort. T2MI was more frequently GCA-related than GCA-unrelated (80% vs. 16.7%, p = 0.080), and GCA diagnosis was the only identified triggering factor in 75% of GCA-related T2MI. GCA-unrelated MI were more frequently T1MI and occurred in patients who had received a higher cumulative dose of prednisone (p = 0.032). GCA was not associated with poorer one-year survival. CONCLUSIONS: GCA-related MI are mainly T2MI probably caused by systemic inflammation rather than coronaritis. GCA-unrelated MI are predominantly T1MI associated with atherothrombotic coronary artery disease.

Published
2021
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4. Temporal Artery Vascular Diseases

Author

Hélène Greigert, André Ramon, Georges Tarris, Laurent Martin, Bernard Bonnotte, and Maxime Samson

Subjects
varicella-zoster virus, giant cell arteritis, temporal arteritis, Medicine, Review, General Medicine, ANCA-associated vasculitis
Abstract

In the presence of temporal arteritis, clinicians often refer to the diagnosis of giant cell arteritis (GCA). However, differential diagnoses should also be evoked because other types of vascular diseases, vasculitis or not, may affect the temporal artery. Among vasculitis, Anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis is probably the most common, and typically affects the peri-adventitial small vessel of the temporal artery and sometimes mimics giant cell arteritis, however, other symptoms are frequently associated and more specific of ANCA-associated vasculitis prompt a search for ANCA. The Immunoglobulin G4-related disease (IgG4-RD) can cause temporal arteritis as well. Some infections can also affect the temporal artery, primarily an infection caused by the varicella-zoster virus (VZV), which has an arterial tropism that may play a role in triggering giant cell arteritis. Drugs, mainly checkpoint inhibitors that are used to treat cancer, can also trigger giant cell arteritis. Furthermore, the temporal artery can be affected by diseases other than vasculitis such as atherosclerosis, calcyphilaxis, aneurysm, or arteriovenous fistula. In this review, these different diseases affecting the temporal artery are described.

Published
2022

5. Hematological malignancies in giant cell arteritis: a french population-based study

Author

Bernard Bonnotte, Georges Tarris, André Ramon, Maxime Samson, Morgane Mounier, Sylvain Audia, Marc Maynadié, Hélène Greigert, Louis Arnould, Catherine Creuzot-Garcher, Laurent Martin, Tibor Ponnelle, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Service de médecine interne et immunologie clinique (SOC 1) [CHU de Dijon], Laboratoire d'Excellence : Lipoprotéines et Santé : prévention et Traitement des maladies Inflammatoires et du Cancer (LabEx LipSTIC), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-Université de Montpellier (UM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Registre des hémopathies malignes de Côte d'Or, Lipides - Nutrition - Cancer [Dijon - U1231] (LNC), Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'Ophtalmologie (CHU de Dijon), Cypath [Dijon], Cypath : siège social [Villeurbanne], Service d'hématologie biologique (CHU de Dijon), Julien, Sabine, and Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement

Subjects
Male, 0301 basic medicine, medicine.medical_specialty, Myeloid, Population, 03 medical and health sciences, 0302 clinical medicine, Rheumatology, immune system diseases, Internal medicine, Epidemiology, medicine, Humans, Pharmacology (medical), cardiovascular diseases, hematological malignancies, [SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory Organs, education, skin and connective tissue diseases, Retrospective Studies, 030203 arthritis & rheumatology, education.field_of_study, business.industry, giant cell arteritis, Incidence, Incidence (epidemiology), Middle Aged, medicine.disease, 3. Good health, Population based study, Giant cell arteritis, 030104 developmental biology, medicine.anatomical_structure, Increased risk, [SDV.MHEP.OS] Life Sciences [q-bio]/Human health and pathology/Sensory Organs, population-based study, Hematologic Neoplasms, cardiovascular system, Female, France, business
Abstract

Objectives An increased risk of haematological malignancies (HM) has been reported in GCA patients. Our study aimed to investigate the incidence and the type of HM occurring in GCA. Methods All patients with GCA and HM living in Côte d’Or (France) were identified by crossing data from the RHEMCO (Registre des Hémopathies Malignes de Côte d’Or) and those having a positive temporal artery biopsy between 1 January 2001 and 31 December 2018. Results Among 276 biopsy-proven GCA patients, 14 HM were identified in 12 patients (4.3%). In comparison with the general population aged >50 y, the incidence of myeloid HM and myeloproliferative syndromes were increased in GCA patients [standardized incidence ratios (SIR) = 2.71 and 5.16, respectively], with a specific increase in men with GCA (SIR = 4.82 and 9.04, respectively) but not in women. In addition, the study of SIR depending on the chronology between GCA and HM diagnoses suggests that there was an increased risk of developing GCA in men but not in women, after a diagnosis of myeloid HM (SIR = 9.56), especially if it was a MPS (SIR = 17.56). Conclusions Our study shows a particular epidemiology of HM in GCA patients, which is characterized by an increased incidence of myeloid HM, especially MPS, in male GCA patients. The chronology of the diagnoses of GCA and HM raises the hypothesis that clonal hematopoiesis may be implicated in some cases of GCA.

Published
2021
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6. Mucosal-associated invariant T cells in giant cell arteritis

Author

Philippe Saas, Sylvain Audia, Claire Gerard, Bernard Bonnotte, Hélène Greigert, Claudie Cladière, T. Ghesquiere, Pierre-Henry Gabrielle, André Ramon, Maxime Samson, Coraline Genet, François Maurier, Georges Tarris, Catherine Creuzot-Garcher, Valérie Quipourt, Paul Ornetti, Hervé Devilliers, Marion Ciudad, Laurent Martin, Agnès Soudry-Faure, Marine Thébault, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Université Bourgogne Franche-Comté [COMUE] (UBFC), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), Hospital Belle Isle, Service de Rhumatologie (CHU de Dijon), Plateforme d’Investigation Technologique [Centre d’Investigation Clinique 1432 module Plurithématique - Dijon] (PIT), Cognition, Action, et Plasticité Sensorimotrice [Dijon - U1093] (CAPS), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre d'Investigation Clinique 1432 (Dijon) - Module Plurithématique : Périnatalité Cancérologie Handicap et Ophtalmologie (CIC-P803), Université de Bourgogne (UB)-Direction Générale de l'Organisation des Soins (DGOS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Direction Générale de l'Organisation des Soins (DGOS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'Ophtalmologie (CHU de Dijon), Délégation à la recherche clinique et à l'innovation [CHU Dijon] (DRCI), Centre d'Investigation Clinique de Besançon (Inserm CIC 1431), Université de Franche-Comté (UFC), and Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])

Subjects
Male, [SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT], Proliferation index, CD3, Biopsy, Immunology, Primary Cell Culture, Stimulation, Mucosal associated invariant T cell, Mucosal-Associated Invariant T Cells, Flow cytometry, Pathogenesis, Tissue Culture Techniques, 03 medical and health sciences, Interferon-gamma, 0302 clinical medicine, medicine, Immunology and Allergy, Humans, Prospective Studies, Cells, Cultured, 030304 developmental biology, Aged, Cell Proliferation, 030203 arthritis & rheumatology, 0303 health sciences, medicine.diagnostic_test, biology, business.industry, giant cell arteritis, Interleukin-18, invariant t-cells, CD28, Middle Aged, medicine.disease, Interleukin-12, Healthy Volunteers, Temporal Arteries, Giant cell arteritis, mucosal associated invariant T, Case-Control Studies, biology.protein, Female, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Signal Transduction
Abstract

International audience; This study aimed to assess the implication of mucosal-associated invariant T (MAIT) cells in GCA. Blood samples were obtained from 34 GCA patients (before and after 3 months of treatment with glucocorticoids (GC) alone) and compared with 20 controls aged >50 years. MAIT cells, defined by a CD3(+)CD4(-)TCRγδ(-)TCRVα7.2(+)CD161(+) phenotype, were analyzed by flow cytometry. After sorting, we assessed the ability of MAIT cells to proliferate and produce cytokines after stimulation with anti CD3/CD28 microbeads or IL-12 and IL-18. MAIT were stained in temporal artery biopsies (TAB) by confocal microscopy. MAIT cells were found in the arterial wall of positive TABs but was absent in negative TAB. MAIT frequency among total αβ-T cells was similar in the blood of patients and controls (0.52 vs. 0.57%; P = 0.43) and not modified after GC treatment (P = 0.82). Expression of IFN-γ was increased in MAIT cells from GCA patients compared to controls (44.49 vs. 32.9%; P = 0.029), and not modified after 3 months of GC therapy (P = 0.82). When they were stimulated with IL-12 and IL-18, MAIT from GCA patients produced very high levels of IFN-γ and displayed a stronger proliferation compared with MAIT from controls (proliferation index 3.39 vs. 1.4; P = 0.032). In GCA, the functional characteristics of MAIT cells are modified toward a pro-inflammatory phenotype and a stronger proliferation capability in response to IL-12 and IL-18, suggesting that MAIT might play a role in GCA pathogenesis. Our results support the use of treatments targeting IL-12/IL-18 to inhibit the IFN-γ pathway in GCA.

Published
2021
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