File:PMC4100089 ijms-15-09184-g001.png

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Attribution 3.0 Unported (CC BY 3.0)

Summary

Author:Mastroianni CM, Lichtner M, Mascia C, Zuccalà P, Vullo V,Department of Public Health and Infectious Diseases, Sapienza University (Openi/National Library of medicine) Source:https://openi.nlm.nih.gov/detailedresult?img=PMC4100089_ijms-15-09184-g001&query=interleukin%20%207%20immune%20system%20inflammation&it=xg&req=4&npos=14 Description:ijms-15-09184-f001: Immunopathogenesis of hepatitis C virus (HCV)-induced liver damage. HCV directlyinteracts with monocytes/macrophage/dendritic cell compartment via CD81 or toll-like receptor (TLR)-7 inducinga pro-inflammatory state and allowing the presentation to naive T and B cells. The increased circulation of chemokines leads to the migration of all these cells into the liver. Natural killer (NK) cells play a central role in control viral replication, but HCV is able to inhibit NK functions. HCV in the liver causes infection of hepatocytes that are a target for the activated effector cells, such as cytotoxic T lymphocytes (CTL), NK, myeloid dendritic cells (mDC) inducing apoptosis. A complex state of chronic immune activation is maintained in the liver and includes also Kupffer cells. In this milieu of pro-inflammatory cytokines (interleukin (IL)-1, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, IL-12) and oxidative stress (ROS), hepatic stellate cells (HSC) are activated to produce extracellular matrix and to induce a dysregulation of the imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs), thus leading to liver fibrosis. Th, T helper; IFN, interferon; sCD, soluble CD; RANTES, regulated on activation normal T cell expressed and secreted; CCR5, C–C chemokine receptor type 5; ECM, extracellular matrix; LPS, lipopolysaccharide; pDC, plasmacytoid dendritic cells; IP, Interferon-gamma-induced protein; TCR, T-cell receptor.