Abstract:

Liver fibrosis is a characterized by activation of hepatic stellate cells (HSCs) that mainly associated with collagen production which initiate the expression of a series of proteins such as the α-smooth muscle actin (α-SMA) protein that causes accumulation of extracellular matrix (ECM) in different regions of the hepatic parenchyma. In worldwide, Liver fibrosis occurs as a result of various chronic liver disorders including steatohepatitis due to viral infections, alcohol intake or metabolic syndrome, autoimmune diseases and cholestasis due to biliary obstruction. Liver fibrosis is an important health problem that results in severe morbidity. The release of inflammatory cells and profibrogenic cytokines collected in the damaged area plays a critical role in the pathogenesis of the disease. Inflammatory response occurs in 3 ways in liver pathogenesis. Type 1 inflammation which is characterized by the production of IL-1β, IL-6, TNF-α and IFN-γ is proinflammatory, anti-fibrogenic and associated with liver inflammation. Type 2 inflammation characterized by the production of IL-4, IL-5, IL-10, IL-13, IL-25 and IL-33 is associated with liver progression and associated with reduced hepatic inflammation. The current theory is that the imbalance between type 1 and type 2 inflammation triggers liver fibrosis. Type 3 inflammation is characterized by IL-17A, IL-17F, IL-22 and IL-26, group 3 initiating lymphoid cell (ILC3), T helper cell 17 (Th17) and T helper cell 22 (Th22). Type 3 cytokines have a pathologically important role in tissue homeostasis. The disorder that occurs in type 3 immunity is associated with abnormal tissue repair, chronic inflammatory diseases, bowel and lung cancers. In our study, we aim to review the role of cytokines in liver fibrosis.

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