Like IL-17, IL-17F is produced by the activated T cells, induces cytokines and chemokines expression and may play a role in skeletal tissue destruction and inflammatory processes in the RA. In arthritis, IL-17 and IL-17F induce significant cartilage matrix release, inhibit new cartilage matrix synthesis and directly regulate cartilage matrix turnover [14]. Both cytokines were also expressed in RA synovial tissue and in RA synoviocytes. They induce a similar expression pattern in the presence of TNF-α; however, IL-17F expression was stronger than IL-17A [20]. IL-17F regulates angiogenesis and production of IL-2, Selleck Panobinostat TNF-β and

TGF-β from endothelial cells [18] and CXCL1, ICAM1, IL-6, IL-8 and G-CSF from epithelial ICG-001 in vivo cells in vitro [17, 21, 22]. The available evidences suggest that IL-17F gene is an excellent candidate gene for chronic inflammatory disease including ulcerative colitis (UC) [23], Bahcet’s disease [24], asthma [25] and inflammatory bowel disease [26]. However, there are

no reports whether IL-17F gene polymorphism is associated with susceptibility to and clinic-pathological features of RA or not. In this study, we examined the association between His161Arg (7488A/G; rs763780) and Glu126Gly (7383A/G; rs2397084) polymorphism of IL-17F gene in Polish patients with RA. Both polymorphisms exist in exon 3. Patients and controls.  A study group consisted of 220 patients with RA (191 women and 29 men) and of 106 healthy individuals without history of diseases with immunological background. All patients fulfilled the American College of Rheumatology (ACR) criteria of 1987 for RA. Patients with RA were recruited from the outpatients and inpatients populations of the Connective Tissue Diseases

Department of the Institute http://www.selleck.co.jp/products/Docetaxel(Taxotere).html of Rheumatology in Warsaw. All patients signed a consent, and clinical data were collected from patients files and questionnaires. The clinical and biochemical characteristics of patients with RA included into the study have been presented in Table 1. The clinical data included: sex, age, disease duration (early RA <1 year and late RA >1 year), number of swollen and tender joints, disease activity score for 28 joints, patients global status and paint, evaluated by the visual analogue scale, range 0–100, functional disability, calculated using the Health Assessment Questionnaires, range 0–3 and radiological progression assessed by a Larsen method. In our study, we compared the frequencies of IL-17F polymorphisms with the highest grade of X-ray changes (0–5) according to Larsen 1995 modification with the use of reference films found in one of the joints assessed in each patient with RA included in the study.