ABSTRACT

Spondyloarthritis encompasses a group of inflammatory disorders characterized by shared pathogenic mechanisms and articular and extraarticular clinical manifestations. Spondyloarthritis is strongly associated with MHC Class I HLA alleles; and both HLA and non-HLA genetic susceptibility factors are associated with increased production of IL-23, increased sensitivity of IL-23R, and IL-17 and TNF associated inflammatory response developing mainly at the entheseal sites and leading to clinical manifestations. IL-17 plays the major role in the inflammatory response and produced by cells of the adaptive and innate immunity. New bone formation develops during the repair phase of enthesitis, which results in bony ankylosis and movement restrictions. Treatments aiming IL-23 and IL-17 cytokines reveals differing efficacy results in findings affecting skin, enthesis and intestine, which suggest a heterogeneity in the regulation of inflammatory response at the tissue level. Further data are needed to plan a phenotype-based treatment aiming precision medicine in spondyloarthritis.