ASSOCIATION BETWEEN DISEASE ACTIVITY AND IL-17A/F, IL-23 AND IL-12/23 (p40) PRODUCTION BY PERIPHERAL BLOOD T LYMPHOCYTES IN BEHCET’S DISEASE

• Published in: The Journal of immunology (1950) Vol. 196; no. 1_Supplement; pp. 194 - 194.4
• Main Authors: Yucel, Aysegul Atak, Sonmez, Cemile, Yesil, Turan Hilmi, Kucuk, Hamit, Mercan, Ridvan, Yucel, Eftal Ahmet, Goker, Berna, Tufan, Muge Aydin, Demirel, Gulderen Yanikkaya, Sezgin, Berna
• Format: Journal Article
• Language: English
• Published: 01-05-2016
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.196.Supp.194.4

Exact pathogenesis of Behcet’s Disease (BD) hasn’t been known but recent studies suggest it’s a genetic-based and immune-related disease. We aimed to investigate the association between disease activity and Th1, Th17 and Treg cells in BD patients via IL-17A/F, IL-23, IL-12/23p40, IL-35 produced by these cells. We also compared our findings with those of SLE patients to investigate their specificity for immunopathogenesis of BD. 15 active and 15 inactive BD patients, 12 active and 12 inactive SLE patients and 12 sex & age-matched healthy controls were involved. Peripheral blood lymphocyte cultures were done. Supernatants from PHA-stimulated and -unstimulated cultures were measured for IL-17A/F, IL-12/23p40, IL-23 and IL-35 levels in time-dependent manner (48 and 72 hrs) by ELISA. For disease activity International Study Group Diagnostic Criteria and SLEDAI index were used for BD and SLE, respectively. IL-17 and IL-23 increased parallelly in both BD and SLE; IL-17 was higher but another Treg cytokine IL-35 was lower in active BD and active SLE compared to healthy controls. After 48 and 72 hrs of PHA stimulation the highest levels of IL-17A/F, IL-22723p40 and IL-23 were measured in active BD followed by active SLE. Our data suggest that IL-17, IL-23 and IL-12/23p40; Th17 and Th1 responses play role in pathogenesis of BD. Finding IL-35 to be lower in active BD compared to inactive BD patients and healthy controls made us think that there can be a plasticity between Th17 and Treg cells depending on disease activity. This is the first time such plasticity is suggested for BD in literature. Our findings also show that IL-17/23 axis contributes to pathogenesis of SLE (another inflammatory rheumatic disease) in addition to other mechanisms like in BD.