Figure 2 Type 3 immunity and AS

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Figure 2 Type 3 immunity and AS Figure 2 | Type 3 immunity and AS. Strong evidence exists for a mucosal origin of type 3 inflammation in patients with ankylosing spondylitis (AS). Paneth cells are an important source of IL-23, which acts on local innate and adaptive lymphocytes to stimulate an IL-17–IL-22 response. These cytokines are considered protective as they promote epithelium integrity. HLA-B27-influenced microbial dysbiosis might drive inflammatory events in the mucosa. IL-17-producing lymphocytes, probably of gut origin, are elevated in the blood of patients with AS. Gut-related trafficking markers, such as α4β7 and CC-chemokine receptor 9 (CCR9) have been implicated in the trafficking of type 3 immune cells into inflamed synovial tissue. Cells involved in type 3 immunity are enriched in different locations of synovial and cartilaginous joints of patients with AS, including synovial fluid, ligaments and subchondral bone marrow. Mechanical stress might drive, in part. the activity of such cells at the enthesis. IL-17 is known to alter the activity of osteoclasts and osteoblasts, probably contributing to aberrant bone formation. APC, antigen-presenting cell; IL7R , interleukin 7 receptor subunit α; ILC3; group 3 innate lymphoid cell; KIR3DL2, immunoglobulin-like receptor 3DL2; MAIT cell, mucosal-associated invariant T cell; NK cell, natural killer cell; TH17 cell, T helper 17 cell. Ranganathan, V. et al. (2017) Pathogenesis of ankylosing spondylitis — recent advances and future directions Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2017.56