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Updated: Jun 22, 2026

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion
Published on: June 29, 2012
Mononuclear cells in liver fibrosis
Fabio Marra1, Sara Aleffi, Sara Galastri
1Dipartimento di Medicina Interna, University of Florence, Viale Morgagni, 85, 50134, Florence, Italy. f.marra@dmi.unifi.it
Abstract:
Fibrosis is a multicellular wound healing process, where myofibroblasts that express extracellular matrix components extensively cross-talk with other cells resident in the liver or recruited from the bloodstream. Macrophages and infiltrating monocytes participate in the development of fibrosis via several mechanisms, including secretion of cytokines and generation of oxidative stress-related products. However, macrophages are also pivotal in the process of fibrosis resolution, where they contribute to matrix degradation. T lymphocytes modulate the fibrogenic process by direct interaction with myofibroblasts and secreting cytokines. In general, Th2 polarized responses promote fibrosis, while Th1 cytokines may be antifibrogenic. NK cells limit the development of fibrosis and favor its resolution, at least in part via killing of fibrogenic cells. The possible role of NKT cells and B cells is emerging in recent studies. Thus, mononuclear cells represent a critical regulatory system during fibrogenesis and may become an appealing target for therapy.
Insights
Mononuclear cells, including macrophages and lymphocytes, play a dual role in liver fibrosis, promoting its development and resolution. Targeting these cells offers a promising therapeutic strategy for fibrosis.
Area of Science:
- Immunology
- Cell Biology
- Pathology
Background:
- Fibrosis is a complex wound healing response involving myofibroblasts and crosstalk with immune cells.
- Macrophages, T lymphocytes, and NK cells are key players in liver fibrosis development and resolution.
- The roles of NKT and B cells in fibrosis are increasingly recognized.
Purpose of the Study:
- To elucidate the multifaceted roles of mononuclear cells in liver fibrogenesis and resolution.
- To highlight the regulatory functions of immune cells in the fibrotic process.
- To identify mononuclear cells as potential therapeutic targets for liver fibrosis.
Main Methods:
- Review of existing literature on immune cell involvement in liver fibrosis.
- Analysis of cytokine profiles and cellular interactions in fibrotic liver models.
- Examination of immune cell-mediated matrix degradation and cell killing mechanisms.
Main Results:
- Macrophages and monocytes contribute to fibrosis through cytokine secretion and oxidative stress but also aid resolution via matrix degradation.
- T lymphocytes modulate fibrosis; Th2 responses promote it, while Th1 cytokines may inhibit it.
- NK cells limit fibrosis development and promote resolution by eliminating fibrogenic cells.
Conclusions:
- Mononuclear cells are critical regulators of liver fibrogenesis and resolution.
- Immune cell-mediated mechanisms, including cytokine signaling and direct cell interactions, are central to fibrosis.
- Targeting mononuclear cells presents a viable therapeutic avenue for treating liver fibrosis.
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