Serum and synovial fluid levels of p40 IL12/23 in spondyloarthropathy patients.
IL-23 is the main inductor in Th17 polarization of naive T cells, inducing IL-17 production. IL-17 has been demonstrated to be elevated in ankylosing spondylitis (AS). The p40 subunit is common to IL-12 and IL-23. We assessed serum and synovial levels of p40 IL12/23 in spondyloarthropathy (SpA) patients and the evolution under anti-TNF. SpA patients fulfilling ESSG criteria were included. Healthy volunteers served as controls. P40 IL12/23 was assessed using Human Quantikine ELISA (R&D Systems), and at the same time, BASDAI, ESR, CRP, IL-17, MMP-3. Patients treated with anti-TNF were evaluated again after 10 weeks of treatment. Statistical analysis used Mann Whitney and correlation tests. Twenty-seven SpA outpatients (20 men), mean age 40.3 years, mean disease duration 10.5 years, HLA B27 positive n = 21, peripheral arthritis n = 8, mean BASDAI 45.7, mean CRP 30.7 mg/l, and 24 controls (12 men), mean age 50.4 years, were included. There is no statistical difference in serum levels of p40IL12/23 between patients (mean 77.8 pg/ml) and controls (103 pg/ml) and between patients with axial and peripheral involvement. Levels were higher in HLA B-27 negative patients (p = 0.02). No statistical correlation was found between p40 IL12/40 serum levels and each of BASDAI, ESR, CRP, serum levels of IL 17, MMP 3. Fourteen AS patients were treated with TNF blockers. Whereas significant reduction in BASDAI, ESR, and CRP were obvious after treatment, there was no significant change in serum level of p40 IL12/23. Mean levels of synovial p40 IL12/23 were higher in SpA patients (n = 6; mean 536 pg/ml) compared to osteoarthritis patients (n = 3; 133 pg/ml) and compared with paired serum SpA levels. These results suggest that serum levels of p40 IL-12/23 may not be considered as a biologic tool of disease activity assessment in SpA patients.
Wendling
Daniel
D
Department of Rheumatology, University Teaching Hospital, Boulevard Fleming, 25030 Besançon, France. dwendling@chu-besancon.fr
Cedoz
Jean-Pierre
JP
Racadot
Evelyne
E
D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D018450:Disease Progression; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D053762:Interleukin-12 Subunit p40 / Q000097:blood* / Q000378:metabolism*; D020381:Interleukin-17 / Q000097:blood; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000097:blood; D008875:Middle Aged; D010003:Osteoarthritis / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D025242:Spondylarthropathies / Q000097:blood* / Q000378:metabolism*; D013582:Synovial Fluid / Q000378:metabolism*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D007074:Immunoglobulin G; D053762:Interleukin-12 Subunit p40; D020381:Interleukin-17; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D019278:Matrix Metalloproteinase 3; D000068879:Adalimumab; D000068800:Etanercept