Estefanía Armas-González1, Ana Díaz-Martín1, María Jesús Domínguez-Luis1, María Teresa Arce-Franco1, Ada Herrera-García1, María Vanesa Hernández-Hernández1, Sagrario Bustabad1, Alicia Usategui1, José L Pablos1, Juan D Cañete1, Federico Díaz-González2. 1. From the Departamento de Farmacología, and Departamento de Medicina, Facultad de Medicina, and Centro para la Investigación Biomédica de las Islas Canarias, Instituto de Investigaciones Biomédicas, Universidad de La Laguna; Servicio de Reumatología, Hospital Universitario de Canarias, Tenerife; Servicio de Reumatología, and Instituto de Investigación, Hospital 12 de Octubre, Madrid; Servicio de Reumatología, Hospital Clinic, Barcelona, Spain.E. Armas-González, PhD; A. Díaz-Martín, PhD, Departamento de Farmacología, Facultad de Medicina, Universidad de La Laguna, and Servicio de Reumatología, Hospital Universitario de Canarias; M.J. Domínguez-Luis, PhD, Centro para la Investigación Biomédica de las Islas Canarias, and Instituto de Investigaciones Biomédicas, Universidad de la Laguna; M.T. Arce-Franco, PhD; A. Herrera-García, PhD; M.V. Hernández-Hernández, MD; S. Bustabad, MD, Servicio de Reumatología, Hospital Universitario de Canarias; A. Usategui, MD, Servicio de Reumatología, Hospital 12 de Octubre; J.L. Pablos, MD, Servicio de Reumatología, and Instituto de Investigación, Hospital 12 de Octubre; J.D. Cañete, MD, Servicio de Reumatología, Hospital Clinic; F. Díaz-González, MD, Departamento de Medicina, Facultad de Medicina, Universidad de La Laguna. 2. From the Departamento de Farmacología, and Departamento de Medicina, Facultad de Medicina, and Centro para la Investigación Biomédica de las Islas Canarias, Instituto de Investigaciones Biomédicas, Universidad de La Laguna; Servicio de Reumatología, Hospital Universitario de Canarias, Tenerife; Servicio de Reumatología, and Instituto de Investigación, Hospital 12 de Octubre, Madrid; Servicio de Reumatología, Hospital Clinic, Barcelona, Spain.E. Armas-González, PhD; A. Díaz-Martín, PhD, Departamento de Farmacología, Facultad de Medicina, Universidad de La Laguna, and Servicio de Reumatología, Hospital Universitario de Canarias; M.J. Domínguez-Luis, PhD, Centro para la Investigación Biomédica de las Islas Canarias, and Instituto de Investigaciones Biomédicas, Universidad de la Laguna; M.T. Arce-Franco, PhD; A. Herrera-García, PhD; M.V. Hernández-Hernández, MD; S. Bustabad, MD, Servicio de Reumatología, Hospital Universitario de Canarias; A. Usategui, MD, Servicio de Reumatología, Hospital 12 de Octubre; J.L. Pablos, MD, Servicio de Reumatología, and Instituto de Investigación, Hospital 12 de Octubre; J.D. Cañete, MD, Servicio de Reumatología, Hospital Clinic; F. Díaz-González, MD, Departamento de Medicina, Facultad de Medicina, Universidad de La Laguna. federico.diaz.gonzalez@gmail.com.
Abstract
OBJECTIVE: To study the qualitative and quantitative phenotypic changes that occur in molecules involved in antigen presentation and costimulation in synovial B cells from rheumatoid arthritis (RA) and psoriatic arthritis (PsA). METHODS: The presence of HLA-DR, CD86, and CD40 in CD20+ cells was studied in RA synovium biopsies using immunohistochemistry and immunofluorescence. Expression was assessed by flow cytometry of the Class II molecules CD40, CD86, CD23, and CD27 on B cells from the synovial fluid (SF), with respect to peripheral blood, from 13 patients with RA and 15 patients with PsA. Expression of interferon-induced protein with tetratricopeptide repeats 4 (IFIT4) in immune-selected CD20+ cells from patients with RA was assessed by quantitative realtime PCR. RESULTS: Infiltrating synovial RA, B cells expressed HLA-DR, CD40, and CD86. Increased expression of CD86, HLA-DR, and HLA-DQ in B cells from SF was found in patients with RA and PsA. HLA-DP was also elevated in rheumatoid SF B cells; conversely, a significantly lower expression was observed in SF from patients with PsA. CD40 expression was increased in SF B cells from PsA, but not in patients with RA. Interestingly, CD20 surface expression level was significantly lower in SF B cells (CD19+, CD138-) from RA, but not in patients with PsA. CD27 upregulation and CD23 downregulation were observed in synovial B cells in both pathologies. Finally, a 4-fold increase in IFIT4 mRNA content was shown in B cells from SF in patients with RA. CONCLUSION: Synovial B cells from patients with RA and patients with PsA express different antigen-presenting cell phenotypes, suggesting that this cell type plays a dissimilar role in the pathogenesis of each disease.
OBJECTIVE: To study the qualitative and quantitative phenotypic changes that occur in molecules involved in antigen presentation and costimulation in synovial B cells from rheumatoid arthritis (RA) and psoriatic arthritis (PsA). METHODS: The presence of HLA-DR, CD86, and CD40 in CD20+ cells was studied in RA synovium biopsies using immunohistochemistry and immunofluorescence. Expression was assessed by flow cytometry of the Class II molecules CD40, CD86, CD23, and CD27 on B cells from the synovial fluid (SF), with respect to peripheral blood, from 13 patients with RA and 15 patients with PsA. Expression of interferon-induced protein with tetratricopeptide repeats 4 (IFIT4) in immune-selected CD20+ cells from patients with RA was assessed by quantitative realtime PCR. RESULTS: Infiltrating synovial RA, B cells expressed HLA-DR, CD40, and CD86. Increased expression of CD86, HLA-DR, and HLA-DQ in B cells from SF was found in patients with RA and PsA. HLA-DP was also elevated in rheumatoid SF B cells; conversely, a significantly lower expression was observed in SF from patients with PsA. CD40 expression was increased in SF B cells from PsA, but not in patients with RA. Interestingly, CD20 surface expression level was significantly lower in SF B cells (CD19+, CD138-) from RA, but not in patients with PsA. CD27 upregulation and CD23 downregulation were observed in synovial B cells in both pathologies. Finally, a 4-fold increase in IFIT4 mRNA content was shown in B cells from SF in patients with RA. CONCLUSION: Synovial B cells from patients with RA and patients with PsA express different antigen-presenting cell phenotypes, suggesting that this cell type plays a dissimilar role in the pathogenesis of each disease.
Entities:
Keywords:
ANTIGEN PRESENTATION; B LYMPHOCYTES; PSORIATIC ARTHRITIS; RHEUMATOID ARTHRITIS
Authors: V Venerito; D Natuzzi; R Bizzoca; N Lacarpia; F Cacciapaglia; G Lopalco; F Iannone Journal: Clin Exp Immunol Date: 2020-05-27 Impact factor: 4.330