We would like

to learn more thank the following funding bodies: Swedish Cancer Foundation, Swedish Science Research Council, Torsten and Ragnar Söderbergs Stiftelser, AFA insurances, ALF: (Avtalet om läkarutbildning och forskning), King Gustav V Stiftelse, Lundbergs Stiftelse, Swedish Medical Society, Gothenburg Medical Society, Reumatikerförbundet, Lundgrens Stiftelse, Amlövs Stiftelser, Adlerbertska stiftelsen, The Royal Society of Arts and Sciences in Gothenburg, Sigurd och Elsa Golje’s minne and the Sahlgrenska Academy. The authors have no conflicting financial interests. “
“Ankylosing spondylitis (AS) is a chronic inflammatory disorder characterized by dysregulated T cells. We hypothesized that the aberrant expression of microRNAs PLX-4720 clinical trial (miRNAs) in AS T cells involved in the pathogenesis of AS. The expression profile

of 270 miRNAs in T cells from five AS patients and five healthy controls were analysed by real-time polymerase chain reaction (PCR). Thirteen miRNAs were found potentially differential expression. After validation, we confirmed that miR-16, miR-221 and let-7i were over-expressed in AS T cells and the expression of miR-221 and let-7i were correlated positively with the Bath Ankylosing Spondylitis Radiology Index (BASRI) of lumbar spine in AS patients. The protein molecules regulated by miR-16, miR-221 and let-7i were measured by Western blotting. We found that the protein levels of Toll-like receptor-4 (TLR-4), a target of let-7i, in T cells from AS patients were decreased. In addition, the mRNA expression of interferon (IFN)-γ was elevated in AS T cells. Lipopolysaccharide (LPS), a TLR-4 agonist, inhibited IFN-γ secretion by anti-CD3+anti-CD28 antibodies-stimulated normal T cells but not AS T cells. In the transfection studies, we found the increased expression of let-7i enhanced IFN-γ production by anti-CD3+anti-CD28+ lipopolysaccharide (LPS)-stimulated normal T cells. In contrast, the decreased expression of let-7i suppressed IFN-γ production by anti-CD3+anti-CD28+ LPS-stimulated AS T cells. In conclusion, we found that miR-16, Oxaprozin miR-221

and let-7i were over-expressed in AS T cells, but only miR-221 and let-7i were associated with BASRI of lumbar spine. In the functional studies, the increased let-7i expression facilitated the T helper type 1 (IFN-γ) immune response in T cells. Ankylosing spondylitis (AS) is a chronic inflammation arthritis that affects both axial and peripheral skeletons and soft tissues. It is conceivable that human leucocyte antigen (HLA)-B27 is the most important risk factor for AS [1], whereas misregulation of T cells could contribute to the inflammatory responses in AS patients [2]. The misfolded HLA-B27 heavy chain homodimer in an animal model has supported the importance of HLA-B27 in the pathogenesis of AS [3]. Subsequent studies have revealed that the activation of Th17 cells is also critical for sustaining the inflammatory responses in AS patients clinically [4-6].