The spectrum of spondyloarthritis is characterized by the intriguing co-occurrence of gut and joint inflammation, although no obvious anatomical link exists. Data from animal models identify stromal cells as important players in pathogenesis, although signalling through TNFRI appeared to be sufficient for development of combined gut and joint inflammation. Interleukin-23 receptor was identified as a susceptibility locus for ankylosing spondylitis. Human genome studies combined with animal model research provide us with new evidence in the fascinating field of the gut-joint axis. However, how these newly identified genetic associations can influence the immunological environment remains to be elucidated.
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