Interleukin 17-expressing Innate Synovial Cells Drive K/BxN Serum-induced Arthritis
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K/BxN serum can induce arthritis in normal mice because of abundant autoantibodies that trigger an innate inflammatory response in joints. To determine whether IL-17 is involved in the pathogenesis of serum-induced arthritis, we injected wild-type and IL-17–/– mice with K/BxN serum and evaluated them for signs of arthritis. Unlike wild-type mice, IL-17–/– mice did not show any signs of arthritis. IL-17 was produced predominantly by CD3– CD4– gdTCR– NK1.1– Sca1int Thy1hi cells residing in the inflamed synovial tissue. When synovial cells extracted from normal joints were stimulated with IL-23 or autoantibody-containing immune complexes, a substantial fraction of Sca1int Thy1hi cells produced IL-17. Thus, we have identified a novel population of IL-17-producing innate synovial cells that play a crucial role in the development of K/BxN serum-induced arthritis.
Abstract
K/BxN serum can induce arthritis in normal mice because of abundant autoantibodies that trigger an innate inflammatory response in joints. To determine whether IL-17 is involved in the pathogenesis of serum-induced arthritis, we injected wild-type and IL-17–/– mice with K/BxN serum and evaluated them for signs of arthritis. Unlike wild-type mice, IL-17–/– mice did not show any signs of arthritis. IL-17 was produced predominantly by CD3– CD4– gdTCR– NK1.1– Sca1int Thy1hi cells residing in the inflamed synovial tissue. When synovial cells extracted from normal joints were stimulated with IL-23 or autoantibody-containing immune complexes, a substantial fraction of Sca1int Thy1hi cells produced IL-17. Thus, we have identified a novel population of IL-17-producing innate synovial cells that play a crucial role in the development of K/BxN serum-induced arthritis.
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