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Results In comparison with RA, synovial infiltration with C-kit positive mast cells was strongly and specifically increased in SpA, independently of the subtype (non-psoriatic versus psoriatic) and disease duration. Staining of mast cell granules with tryptase and toluidine blue as well as analysis of synovial fluid levels of histamine and tryptase did not indicate increased degranulation in SpA synovitis. Mast cells expressed significantly more IL-17 in SpA than RA synovitis and constituted the major IL-17 expressing cell population in SpA synovitis. Targeting mast cells with the c-kit inhibitor imatinib mesylate in ex vivo tissue cultures led to a significant decrease in the production of IL-17 as well as other pro-inflammatory cytokines. To confirm that mast cell infiltration is not a merely secondary, inflammationdependent feature of SpA, we assessed the impact of TNF blockade on mast cell infiltration in vivo. Analysis of paired synovial biopsies before and after treatment revealed that neither the number of mast cells nor the expression of IL-17 by mast cells was affected by effective TNF blockade in SpA.

IL-17 producing mast cells contribute to synovial inflammation in non-psoriatic and psoriatic spondyloarthritis