Melanoma may be preventable by regular sunscreen use in adults.

Objective. The spondylarthritides (SpA), including ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, and arthritis associated with inflammatory bowel disease, cause chronic inflammation of the large peripheral and axial joints, eyes, skin, ileum, and colon. Genetic studies reveal common candidate genes for AS, PsA, and Crohn's disease, including IL23R, IL12B, STAT3, and CARD9, all of which are associated with interleukin-23 (IL-23) signaling downstream of the dectin 1 ␤-glucan receptor. In autoimmune-prone SKG mice with mutated ZAP-70, which attenuates T cell receptor signaling and increases the autoreactivity of T cells in the peripheral repertoire, IL-17-dependent inflammatory arthritis developed after dectin 1-mediated fungal infection. This study was undertaken to determine whether SKG mice injected with 1,3-␤-glucan (curdlan) develop evidence of SpA, and the relationship of innate and adaptive autoimmunity to this process.Methods. SKG mice and control BALB/c mice were injected once with curdlan or mannan. Arthritis was scored weekly, and organs were assessed for pathologic features. Anti-IL-23 monoclonal antibodies were injected into curdlan-treated SKG mice. CD4؉ T cells were transferred from curdlan-treated mice to SCID mice, and sera were analyzed for autoantibodies.Results. After systemic injection of curdlan, SKG mice developed enthesitis, wrist, ankle, and sacroiliac joint arthritis, dactylitis, plantar fasciitis, vertebral inflammation, ileitis resembling Crohn's disease, and unilateral uveitis. Mannan triggered spondylitis and arthritis. Arthritis and spondylitis were T cell-and IL-23-dependent and were transferable to SCID recipients with CD4؉ T cells. SpA was associated with collagen-and proteoglycan-specific autoantibodies.Conclusion. Our findings indicate that the SKG ZAP-70 W163C mutation predisposes BALB/c mice to SpA, resulting from innate and adaptive autoimmunity, after systemic ␤-glucan or mannan exposure.The spondylarthritides (SpA) comprise a group of diseases, including ankylosing spondylitis (AS), psoriatic arthritis (PsA), and reactive arthritis, that cause chronic joint inflammation and extraarticular inflammatory manifestations, including anterior uveitis, psoriasis, and the inflammatory bowel diseases (IBD) Crohn's disease and ulcerative colitis. SpA are thought to be

Results. In curdlan-treated SKG mice, arthritis, enthesitis, and ileitis were IL-23 dependent. Enthesitis was specifically dependent on IL-17A and IL-22. IL-23 was induced in the ileum, where it amplified ER stress, goblet cell dysfunction, and proinflammatory cytokine production. IL-17A was pathogenic, while IL-22 was protective against ileitis. IL-22؉CD3؊ innate-like cells were increased in lamina propria mononuclear cells of ileitis-resistant BALB/c mice, which developed ileitis after curdlan injection and anti-IL-22.Conclusion. In response to systemic ␤-1,3-glucan, intestinal IL-23 provokes local mucosal dysregulation and cytokines driving the SpA syndrome, including IL-17/IL-22-dependent enthesitis. Innate IL-22 production promotes ileal tolerance.