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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Nat Immunol. 2016 Nov 7;18(1):104–113. doi: 10.1038/ni.3579

Figure 1. IL-23 contributes to the initiation but not the effector phase of autoantibody-mediated arthritis.

Figure 1

(a) Clinical arthritis scores of C57BL/6 wild-type (WT) mice (n = 7) and Il23a−/− mice (n = 6) after the induction of CIA (left), summarized as area under the curve (AUC) (middle), and microscopy of the ankle joints of such mice, stained for tartrate-resistant acid phosphatase for visualization of osteoclast formation and joint destruction (right) (n ≥ 5 mice per genotype). (b) Clinical arthritis scores of K/BxN mice treated with neutralizing antibody to IL-23p19 (α-IL-23) (n = 10 mice) or isotype-matched control antibody (Isotype) (n = 11 mice) (left and middle, presented as in a), and microcopy of ankle joints, stained as in a (n ≥ 5 mice per group) (right). (c,d) Clinical arthritis scores of wild-type mice (n = 4) and Il23a−/− mice (n = 5) that received CII-specific antibodies (c) or wild-type mice that received serum from arthritic K/BxN mice together with a neutralizing antibody to IL-23p19 (n = 3 mice) or isotype-matched control antibody (n = 5 mice). Scale bars (a,b), 100 μm. Each symbol (middle (a,b) or right (c,d)) represents an individual mouse. P = 0.89 (c) and P = 0.98 (d); *P ≤ 0.01 and **P ≤ 0.001 (Student’s t-test). Data are representative of at least three independent experiments (error bars, s.e.m.).