Rehaume LM, et al. - Researchers restrained IL-23 in dysbiotic ZAP-70-mutant SKG mice [developed interleukin (IL)-23-dependent spondyloarthropathy (SpA)-like arthritis, psoriasis-like skin inflammation, and Crohn’s-like ileitis in response to microbial beta 1,3-glucan (curdlan)] to analyze the relationship between host IL-23 signaling and gut bacterial dysbiosis in SpA. They observed a decrease in Bacteroidaceae, Porphyromonadaceae, and Prevotellaceae after inhibiting IL-23p19 in naive SKG mice. An inclination in abundance of Clostridiaceae and Lachnospiraceae families and a concomitant decrease was observed in curdlan-mediated SpA development. They noted a relationship between the relative abundance of specific pathobionts with disease severity.