Title: Proinflammatory T helper 17 cells are expanded and induced by dendritic cells in spondyloarthritis-prone HLA-B27 transgenic rat
Authors: Glatigny, Simon
Fert, Ingrid
Blaton, Marie A
Lories, Rik
Araujo, Luiza M
Chiocchia, Gilles
Breban, Maxime # ×
Issue Date: Jan-2012
Publisher: John Wiley & Sons
Series Title: Arthritis and Rheumatism vol:64 issue:1 pages:110-120
Article number: 10.1002/art.33321
Abstract: OBJECTIVE: HLA-B27/human β2-microglobulin transgenic (B27) rats, a model of spondyloarthritis, develop spontaneous colitis and arthritis under conventional conditions. CD4(+) T cells are pivotal for the development of inflammation in B27 rats. The aim of this study was to characterize the phenotype of CD4(+) T cells in this model and to determine if dendritic cells (DCs) can induce proinflammatory T cells. METHODS: The phenotype of CD4(+) T cells from the lymph nodes draining the inflammatory sites was analyzed by flow cytometry. Immunostaining was used to detect IL-17-producing cells in joints. Co-cultures of DCs from B27 or control rats (transgenic for HLA-B7 or nontransgenic) with control CD4(+) T cells were performed with anti-TCRαβ stimulation. RESULTS: IL-17A- and TNFα-producing CD4(+) T cells were expanded in mesenteric and popliteal lymph nodes from B27 rats. The accumulation of Th-17 cells correlated with disease development, in contrary to Th-1 or Treg cells. IL-17 positive mononuclear cells were detected in arthritic joints of B27 but not in control joints. Finally, in vitro co-cultures demonstrated that DCs from disease-prone rats preferentially induced Th-17 differentiation in CD4(+) T cells, in a contact-dependent manner which may involve defective co-stimulatory molecules engagement. CONCLUSION: Expanded CD4(+) T cells in B27 rats exhibit a pro-inflammatory Th-17 phenotype characterized by IL-17A and TNFα production. Furthermore, this population is preferentially induced by DCs from B27 rats. All these data point towards an induction of Th-17 cells as a possible pathogenic mechanism in this model of spondyloarthritis. However, their pathogenic role still needs to be shown.
ISSN: 0004-3591
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Rheumatology Section (-)
× corresponding author
# (joint) last author

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