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Fig. 1 | Arthritis Research & Therapy

Fig. 1

From: Targeting inflammatory pathways in axial spondyloarthritis

Fig. 1

Inflammatory Pathways in axSpA. In spondyloarthritis, biomechanical stress and inflammatory factors, including infectious antigens, amplified by MHC susceptibility genes, HLA-B27 variants, and ERAP1 SNP transcription factors induce specific cell types to produce a series of inflammatory cytokines, including IL-23, IL-17, TNF, IL-1, and IL-6. Hematopoietic stem cells elaborate NF-κB, RANKL, and M-CSF to differentiate monocytes to osteoclasts, which extend inflammatory damage in the supporting structures of the sacroiliac and peripheral joints. Mesenchymal stem cells facilitated by Wnt and BMP differentiate to osteoblasts to form new bone and ankyloses. BMP, bone morphogenetic protein; CRP, C-reactive protein; DKK, Dickkopf; HLA, human leukocyte antigen; ERAP1, endoplasmic reticulum aminopeptidase 1; IL, interleukin; ILC-3s, group 3 innate lymphoid cells; M-CSF, monocyte colony-stimulating factor; MMP, metalloproteinase; NF-κB, nuclear factor-κB; OPG, osteoprotegerin; OSX, osterix zinc finger-containing transcription factor; RANKL, receptor activator of nuclear factor-κB ligand; RUNX, runt-related transcription factor; SFRP, secreted frizzled-related proteins; SNP, single-nucleotide polymorphism; SOX9, sex-determining region Y transcription factor; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor. Italicized = transcription factor; red = inflammation; blue = bone formation/ankylosis. Th1 cells = T helper cells for humoral immunity; Th17 cells = T helper cells for IL-17 inflammation, damage

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