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Mucosal-associated invariant T cells in Giant Cell Arteritis.
Ghesquière, Thibault; Ciudad, Marion; Ramon, André; Greigert, Hélène; Gerard, Claire; Cladière, Claudie; Thébault, Marine; Genet, Coraline; Devilliers, Hervé; Maurier, François; Ornetti, Paul; Quipourt, Valérie; Gabrielle, Pierre-Henry; Creuzot-Garcher, Catherine; Tarris, Georges; Martin, Laurent; Soudry-Faure, Agnès; Saas, Philippe; Audia, Sylvain; Bonnotte, Bernard; Samson, Maxime.
Afiliación
  • Ghesquière T; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Ciudad M; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Ramon A; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France; Department of Rheumatology, Dijon University Hospital, Dijon, France.
  • Greigert H; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Gerard C; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Cladière C; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Thébault M; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Genet C; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Devilliers H; Department of Internal Medicine and Systemic Diseases, Dijon University Hospital, Dijon, France.
  • Maurier F; Department of Internal Medicine, Hospital Belle Isle, Metz, France.
  • Ornetti P; Department of Rheumatology, Dijon University Hospital, Dijon, France; CIC-1432 Plateforme d'investigation Technologique Dijon University Hospital, INSERM UMR1093-CAPS, Université Bourgogne, Dijon, France.
  • Quipourt V; Department of Internal Medicine and Geriatrics, Dijon University Hospital, Dijon, France.
  • Gabrielle PH; Department of Ophtalmology, Dijon University Hospital, Dijon, France.
  • Creuzot-Garcher C; Department of Ophtalmology, Dijon University Hospital, Dijon, France.
  • Tarris G; Department of Pathology, CHU François Mitterrand, Dijon, France.
  • Martin L; Department of Pathology, CHU François Mitterrand, Dijon, France.
  • Soudry-Faure A; Unité de Soutien Méthodologique, DRCI, Dijon Bourgogne University Hospital, 21000, Dijon, France.
  • Saas P; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France; CIC-1431, INSERM, Besançon University Hospital, EFS Bourgogne Franche-Comté, LabEx LipSTIC, F-25000, Besançon, France.
  • Audia S; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Bonnotte B; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France.
  • Samson M; Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France; Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-21000, Dijon, France. Electronic address: maxime.samson@u-bourgo
J Autoimmun ; 121: 102652, 2021 07.
Article en En | MEDLINE | ID: mdl-34000675
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 αß-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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arteritis de Células Gigantes / Células T Invariantes Asociadas a Mucosa Tipo de estudio: Observational_studies / Risk_factors_studies Límite: Aged / Female / Humans / Male / Middle aged Idioma: En Revista: J Autoimmun Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2021 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arteritis de Células Gigantes / Células T Invariantes Asociadas a Mucosa Tipo de estudio: Observational_studies / Risk_factors_studies Límite: Aged / Female / Humans / Male / Middle aged Idioma: En Revista: J Autoimmun Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2021 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido