We are analyzing https://link.springer.com/article/10.1186/ar3870.

Title:
Interleukin-7-aggravated joint inflammation and tissue destruction in collagen-induced arthritis is associated with T-cell and B-cell activation | Arthritis Research & Therapy
Description:
Introduction We sought to investigate the capacity of interleukin (IL)-7 to enhance collagen-induced arthritis and to study by what mechanisms this is achieved. Methods Mice received multiple injections with IL-7 or phosphate-buffered saline (PBS) as a control. Arthritis severity and incidence were determined by visual examination of the paws. Joint destruction was determined by assessing radiographs and immunohistochemistry of the ankle joints. Total cellularity and numbers of T-cell and B-cell subsets were assessed, as well as ex vivo production of interferon-γ (IFN-γ), IL-17, and IL-4. Proinflammatory mediators were measured in serum with multianalyte profiling. Results IL-7 increased arthritis severity and radiology-assessed joint destruction. This was consistent with IL-7-increased intensity of cell infiltrates, bone erosions, and cartilage damage. Splenic CD19+ B cells and CD19+/GL7+ germinal center B cells, as well as CD4 and CD8 numbers, were increased by IL-7. IL-7 expanded memory T cells, associated with increased percentages of IFN-γ-, IL-4-, and IL-17-producing CD4+ T cells. On antigen restimulation of draining lymph node cells in vitro IL-7 treatment was found to increase IFN-γ and IL-17 production, whereas IL-4 was reduced. IL-7 also increased concentrations of proinflammatory mediators, indicative of T-cell activation (sCD40L), vascular activation (VCAM-1, VEGF), tissue destruction (fibroblast growth factor-basic (FGF-b), LIF), and chemotaxis (MIP-1γ, MIP-3β, lymphotactin, MDC, and MCP-5). Conclusions In arthritic mice, IL-7 causes expansion of T and B cells, associated with increased levels of proinflammatory mediators. IL-7 intensifies arthritis severity and joint destruction, accompanied by increased Th1 and Th17 activity. These data indicate that IL-7 could be an important mediator in arthritic conditions and that targeting IL-7 or its receptor represent novel therapeutic strategies.
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Keywords {🔍}

cells, arthritis, mice, increased, pubmed, article, activation, google, scholar, cas, cell, interleukin, factor, figure, destruction, numbers, joint, tcell, compared, bone, expression, significantly, pbs, activity, production, tissue, patients, rheumatoid, data, severity, day, central, inflammation, mediators, treatment, receptor, cytokines, group, van, concentrations, growth, levels, collageninduced, bijlsma, study, proinflammatory, cartilage, ilr, lafeber, roon,

Topics {✒️}

monocyte-dependent b-cell activation il-7r-induced t-cell activation stat3/il-7-dependent homeostatic proliferation anti-cd19 peridinin-chlorophyll-protein inhibit t-cell-driven inflammation van roon ja interleukin-7-aggravated joint inflammation inducing t-cell-related cytokines cell-dependent osteoclast activity/formation il-7r-mediated immune activation macrophage-colony-stimulating factor van roon jag leukemia inhibitory factor dab+substrate-chromagen system radiology-assessed joint destruction cytokine-secreting t-helper cells inguinal-draining lymph nodes blocking tslp-induced signaling cd3+ t-cell counts fibroblast growth factor-basic enhance collagen-induced arthritis rabbit polyclonal anti-cathepsin article download pdf wenting-van wijk mw prepare single-cell suspensions enzyme-linked immunosorbent assay anti-ifn-γ fitc il-7 induces t-cell endothelial cell adhesion macrophage inflammatory protein poorly proliferating il-7rlow/ contact-dependent activation increased ifn-γ production cd19+/gl7+ germinal center local antigen-driven responses anti-cd8 pacific blue sarita ay hartgring reduced b-cell activity leukaemia inhibitory factor cells producing ifn-γ monocyte/macrophage activation collagen-induced arthritis epidermal growth factor acute-phase reactant acute-phase reactants reduced t-cell numbers tumor necrosis factor fibroblast growth factor including rheumatoid arthritis il-7 receptor-α chain

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WebPage:
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         headline:Interleukin-7-aggravated joint inflammation and tissue destruction in collagen-induced arthritis is associated with T-cell and B-cell activation
         description:We sought to investigate the capacity of interleukin (IL)-7 to enhance collagen-induced arthritis and to study by what mechanisms this is achieved. Mice received multiple injections with IL-7 or phosphate-buffered saline (PBS) as a control. Arthritis severity and incidence were determined by visual examination of the paws. Joint destruction was determined by assessing radiographs and immunohistochemistry of the ankle joints. Total cellularity and numbers of T-cell and B-cell subsets were assessed, as well as ex vivo production of interferon-γ (IFN-γ), IL-17, and IL-4. Proinflammatory mediators were measured in serum with multianalyte profiling. IL-7 increased arthritis severity and radiology-assessed joint destruction. This was consistent with IL-7-increased intensity of cell infiltrates, bone erosions, and cartilage damage. Splenic CD19+ B cells and CD19+/GL7+ germinal center B cells, as well as CD4 and CD8 numbers, were increased by IL-7. IL-7 expanded memory T cells, associated with increased percentages of IFN-γ-, IL-4-, and IL-17-producing CD4+ T cells. On antigen restimulation of draining lymph node cells in vitro IL-7 treatment was found to increase IFN-γ and IL-17 production, whereas IL-4 was reduced. IL-7 also increased concentrations of proinflammatory mediators, indicative of T-cell activation (sCD40L), vascular activation (VCAM-1, VEGF), tissue destruction (fibroblast growth factor-basic (FGF-b), LIF), and chemotaxis (MIP-1γ, MIP-3β, lymphotactin, MDC, and MCP-5). In arthritic mice, IL-7 causes expansion of T and B cells, associated with increased levels of proinflammatory mediators. IL-7 intensifies arthritis severity and joint destruction, accompanied by increased Th1 and Th17 activity. These data indicate that IL-7 could be an important mediator in arthritic conditions and that targeting IL-7 or its receptor represent novel therapeutic strategies.
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