Purpose of review <p>Spondyloarthritis animal models such as the HLA-B27 transgenic rat, SKG mouse and cytokine overexpression models have proven useful for testing hypotheses regarding pathogenesis. Recent developments in the field from human studies have shifted attention to HLA-B2705 restricted CD8+ T cell clonotype expansion and the “arthritogenic peptide” theory. Since human and rodent MHC and T cell compartments differ, translatability comes into question. In this review, we will discuss the advantages and caveats of several spondyloarthritis rodent models. We will review classic studies and more recent reports providing insight into pathologic T cells outside the canonical paradigm of MHC Class I-CD8+ T cell interaction.</p> Recent findings <p>Animal models have revealed requisite “ingredients’ for a spondyloarthritis phenotype, including inflammatory mediators and lymphoid cell types. Most of these models highlight the role of Th17 cells and other IL-17 producing cells. Indeed, the IL-23 minicircle model directly led to the identification of IL-17 producing γδ T cells in typical spondyloarthritis anatomic locations. In addition to identifying lymphocyte players, animal models have elucidated T cell regulation, including innate immune (e.g. neutrophil) T cell crosstalk and gut-joint trafficking. Current studies are also beginning to clarify roles for innate lymphocytic cells such as MAIT and iNKT cells.</p> Summary <p>Animal model studies have provided vital insight into T cell pathogenic mechanisms outside canonical MHC Class I-CD8 interaction. Many of these findings have been replicated in human subjects. Furthermore, work from animal models directly supported the development of IL17 and IL23 targeting therapeutics, attesting to their relevance. Main text: (~ 4246 words), 1 Figure and 1 Table.</p>