Analysis of IL-17.sup.+ .sup.cells in facet joints of patients with spondyloarthritis suggests that the innate immune pathway might be of greater relevance than the Th17-mediated adaptive immune response

Introduction In this study, we analysed the number of IL-17.sup.+ .sup.cells in facet joints, in the peripheral blood (PB) and synovial fluid (SF) of spondyloarthritis (SpA) patients and compared these results with those of patients with other rheumatic diseases and controls. Methods Immunohistochemical analysis of IL-17.sup.+ .sup.cells was performed in facet joints of 33 ankylosing spondylitis (AS) patients and compared with data from 20 osteoarthritis (OA) patients. The frequency of IL-17.sup.+.sup.CD4.sup.+ .sup.T cells in PB and SF of SpA patients (PB n = 30, SF n = 11), rheumatoid arthritis (RA) patients (PB n = 14, SF n = 7), OA patients (PB n = 10) and healthy controls (PB n = 12) was analysed after stimulation with Staphylococcus aureus Enterotoxin B and phorbol 12-myristate 13-acetate/ionomycin and quantified by flow cytometry. Results In AS facet joints, the frequency of IL-17-secreting cells was significantly higher than in samples obtained from OA patients (P [less than] 0.001), with a slight predominance of IL-17.sup.+ .sup.cells among the mononuclear cells (61.5% [+ -] 14.9%) compared to cells with polysegmental nuclei. Immunofluorescence microscopy revealed that the majority of IL-17.sup.+ .sup.cells were myeloperoxidase-positive (35.84 [+ -] 13.06/high-power field (HPF) and CD15.sup.+ .sup.neutrophils (24.25 [+ -] 10.36/HPF), while CD3.sup.+ .sup.T cells (0.51 [+ -] 0.49/HPF) and AA-1.sup.+ .sup.mast cells (2.28 [+ -] 1.96/HPF) were less often IL-17-positive. The frequency of IL-17.sup.+.sup.CD4.sup.+ .sup.T cells in the PB and SF of SpA patients did not differ significantly compared to RA patients, OA patients or healthy controls. Conclusions Our data suggest an important role for IL-17 in the inflammatory processes in AS. However, the innate immune pathway might be of greater relevance than the Th17-mediated adaptive immune response.