Fig. 1

IL-17A-deficient mice induced with serum transfer arthritis develop similar inflammation and bone erosion, but increased periosteal bone. a Clinical inflammation scores and change in ankle thickness in IL-17A-deficient (IL-17A knockout (KO)) and wild-type mice. Values are the mean ± SEM (n = 24 mice per group, days 0–10; n = 12 mice per group, days 11–14). b Representative serial H&E-stained and tartrate-resistant alkaline phosphatase (TRAP)-stained sections of the navicular bone of IL-17A-deficient and wild-type mice. Scale bar represents 100 μm. c Histopathologic scoring of inflammation and bone erosion of the ankle and midfoot regions in IL-17A-deficient and wild-type mice at peak inflammation. Each symbol represents the mean histologic score per mouse (n = 8 mice per group; non-responders with inflammation scores ≤ 0.5 were removed). Horizontal lines represent the group means. d Schematic of the murine ankle and foot. Red arrows indicate reproducible sites of periosteal bone formation in serum transfer arthritis (STA) at the mid and distal tibia and navicular bone. e Representative H&E-stained sections of the tibia (left panels) and navicular bone (middle and right panels) of IL-17A-deficient and wild-type mice. Scale bar represents 100 μm. Arrows indicate areas of periosteal new bone formation. *Tendon inserting on tibia at site of bone formation. f Quantitation of the volume of periosteal bone formation at peak inflammation in IL-17A-deficient and wild-type mice. Data represent the mean ± SEM (n = 8 mice per group) (*p < 0.05)