MONONUCLEAR CELL INFILTRATION ACCOMPANIED BY THE PROGRESSION OF FIBROTIC AND CIRRHOTIC TRANSFORMATIONS IN THE LIVER TISSUE

Abstract

Fibrosis is a complex, multicellular wound-healing response, where myofibroblasts—key producers of extracellular matrix (ECM)—actively interact with both liver-resident cells and those recruited from the circulation. Macrophages and infiltrating monocytes contribute to fibrogenesis through multiple pathways, including cytokine secretion and the production of reactive oxygen species. Interestingly, these same macrophages also play a crucial role in fibrosis resolution by facilitating ECM degradation. T lymphocytes influence fibrosis progression by interacting directly with myofibroblasts and releasing various cytokines. Typically, a Th2-skewed immune response supports fibrotic activity, whereas Th1-associated cytokines may exert antifibrotic effects. Natural killer (NK) cells help to restrain fibrosis and promote its regression, partly by inducing apoptosis in activated fibrogenic cells. Recent studies also point to a potential role for NKT and B cells in modulating liver fibrogenesis. Overall, mononuclear immune cells serve as key regulators of the fibrotic process and represent promising targets for therapeutic intervention.