TY - JOUR T1 - Expression profiling of Th17 cell activators revealed elevation of STAT-3 in progressing sarcoidosis JF - European Respiratory Journal JO - Eur Respir J VL - 38 IS - Suppl 55 SP - p4762 AU - Regina Fillerova AU - Eva Kriegova AU - Tereza Tomankova AU - Frantisek Mrazek AU - Monika Zurkova AU - Vitezslav Kolek AU - Martin Petrek Y1 - 2011/09/01 UR - http://erj.ersjournals.com/content/38/Suppl_55/p4762.abstract N2 - Sarcoidosis is a Th1/Th17 multisystem inflammatory disorder of unknown aetiology. Although Th17 cells have been implicated in sarcoidosis and its progression, there is limited information about the molecules involved in the Th17 immune response in sarcoidosis and its phenotypes.We, therefore, investigated, mRNA expression of Th17 pathway activators (IL-6, IL-21, IL-23, TGFbeta, RORC, STAT-3) together with the cytokines produced by Th17 cells (IL-17A, IL-17F, IL-22) by quantitative RT-PCR in bronchoalveolar (BAL) cells from 77 sarcoidosis patients (S) and 20 control subjects (C); subanalysis was performed in sarcoid phenotypes.Of studied Th17 activators, IL-6 (mean S/C; 0.37/0.04, p=0.0001), IL-21 (0.002/0.001, p=0.001), IL-23 (0.06/0.02, p=0.001), TGFbeta (0.86/0.51, p=0.02) and RORC (0.06/0.02, p=0.0002) were up-regulated in sarcoidosis vs. controls. Expression of Th17 cytokines did not differ between sarcoidosis and controls (p>0.05). The expression profiling in remitting (n=27) and progressing (n=40) sarcoidosis, as assessed by the disease outcome after 2 years, revealed elevation of STAT-3 in progressing sarcoidosis (p=0.01).In conclusion, increased expression of Th17 activators (IL-6, IL-21, IL-23, TGFbeta, RORC) was observed in sarcoid BAL cells irrespective of clinical phenotype. Enhanced expression of STAT-3, an essential regulator of Th17 cells, was detected in patients with progressing sarcoidosis. Further studies on the role of STAT-3 and Th17 cells in the progression towards the fibrosis in sarcoidosis are needed.Grant support: IGA MZ CR NS/11117, IGA MZ CR NS/10267, PU LF_2010_008. ER -