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Human Th17 pro-inflammatory cells are currently defined as cells that produce IL-17A and F, tumor necrosis factor (TNF)-a, IL-6, IL-21, IL-22 and IL-23. Recently discovered related molecules are forming a family of cytokines, the IL-17 family, IL-17A, IL-17B, IL-17C, IL-17D, IL-17E and IL-17F . The associated receptors for the IL-17 family identified are IL-17R, IL-17RH1, IL-17RL (receptor like), IL-17RD and IL-17RE. This review introduces the roles of IL-17 and Th17 cells in human autoimmune diseases. Studies have shown that T cells with inflammatory effects on epithelial, endothelial and fibroblast cells express IL-17. Th17 cells are supposed to be involved in various autoimmune diseases, such as rheumatoid arthritis, psoriasis, multiple sclerosis, and inflammatory bowel diseases. Base on the biologic functions and regulation, IL-17 has regulatory roles in host defense and chronic inflammation which result in tissue damage and autoimmunity. So the IL-17 links links innate and adaptive immunity and has both beneficial and pathological effects on the immune system. This paper will focus on the possible roles of IL-17 in autoimmune diseases, a fundamental player in immune regulation. [ABSTRACT FROM AUTHOR]

Introduction: Psoriasis is a chronic, inflammatory, T-cell-mediated and hyperproliferative skin disease characterized by erythematous, squamous, sharply circumscribed and infiltrated plaques. The metabolisms of the collagen proteins undergo considerable changes due to the acceleration of their turnovers as a result of increased prolidase activity in psoriasis patients. Aim: To determine the level of prolidase activity in psoriasis patients and evaluate its relationship with the oxidative system. Material and methods: The serum prolidase enzyme activity, total antioxidant levels and total oxidant levels of 40 psoriasis patients and a control group including 47 healthy individuals were analyzed by using their serum samples, and their oxidative stress indices were calculated. Results: The prolidase levels (p < 0.01), total oxidant levels (p < 0.01) and oxidative stress index levels (p < 0.001) of the patient group were higher than the corresponding parameters in the control group. The total antioxidant level was low (p < 0.01). Although a positive correlation was found between the prolidase and total antioxidant levels and the total oxidant level, no correlation was found between prolidase and the oxidative stress index. Conclusions: It has been determined that the activity of the prolidase enzyme increases due to the increased collage turnover in psoriasis patients. Increased serum oxidant levels and oxidative stress indices values may play a role in the pathogenesis of psoriasis. [ABSTRACT FROM AUTHOR]

Introduction: Recruitment of the inflammatory cells from blood to the airways in asthma is mediated by adhesive molecules, e.g. selectins and integrins. The most important integrins in cells trafficking are molecules containing α4 and β2 subunits. We hypothesized that also α1β1 and α2β1 integrins (both found by us on blood eosinophils of asthmatic subjects) are important in asthma pathogenesis. Aim: To assess the expression of selected very late antigen (VLA) subunits (α1, α2, α4 and β1) on blood CD4 and CD8 T lymphocytes from stable atopic asthmatic patients. Material and methods: The study was conducted on 25 adult atopic asthmatics (mild to moderate persistent asthma in a stable clinical condition) and 17 matched healthy controls using flow cytometry. Results: Expression of α4 and β1 on CD4 T cells was significantly higher in asthma than in controls. The α1 subunit was absent from blood lymphocytes. The α2 chain hardly detected on lymphocytes from healthy subjects was distinctively present in asthmatics. Surprisingly, in subjects suffering from asthma for longer than 4 years (n = 15), the overexpression of α2, α4 and β1 was observed on both: CD4 and CD8 T cells. Conclusions: Expression of selected VLA subunits on blood T cells may depend on asthma duration. The biological role of α2β1 integrin in asthma is unknown, but as it was described as a stimulator of collagen accumulation in the airways, α2β1 integrin could be, at least in part, responsible for asthma airway remodelling. [ABSTRACT FROM AUTHOR]