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Fig. 7 | Arthritis Research & Therapy

Fig. 7

From: Blockade of bone morphogenetic protein signaling potentiates the pro-inflammatory phenotype induced by interleukin-17 and tumor necrosis factor-α combination in rheumatoid synoviocytes

Fig. 7

Schematic representation of BMP involvement in rheumatoid arthritis pathogenesis. Under steady-state conditions, autocrine BMP production could downregulate the expression and contribute to keep low levels of pro-inflammatory cytokines and chemokines as well as matrix metalloproteinases in synoviocytes. In the presence of increased levels of TNF-α and IL-17, synoviocytes become activated and enhance the production of BMPs which, however, could no longer control the levels of pro-inflammatory and pro-destructive factors because of the simultaneous upregulated expression of BMP signaling inhibitors in synoviocytes. Increased levels of BMPs could then participate in the recruitment and activation of immune cells contributing to rheumatoid arthritis along with the increased levels of pro-inflammatory cytokines, chemokines, and metalloproteinases. BMP bone morphogenetic protein, CCL2 chemokine (C-C motif) ligand 2, CCL5 chemokine (C-C motif) ligand 5, GM-CSF granulocyte-macrophage colony-stimulating factor, IL interleukin, MMP matrix metalloproteinase, TNF-α tumor necrosis factor-alpha

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