Abstract
Mast cells (MCs) are immune cells of the myeloid lineage that are present in the connective tissue throughout the body and in mucosa tissue. They originate from hematopoietic stem cells in the bone marrow and circulate as MC progenitors in the blood. After migration to various tissues, they differentiate into their mature form, which is characterized by a phenotype containing large granules enriched in a variety of bioactive compounds, including histamine and heparin. These cells can be activated in a receptor-dependent and -independent manner. Particularly, the activation of the high-affinity immunoglobulin E (IgE) receptor, also known as FcεRI, that is expressed on the surface of MCs provoke specific signaling cascades that leads to intracellular calcium influx, activation of different transcription factors, degranulation, and cytokine production. Therefore, MCs modulate many aspects in physiological and pathological conditions, including wound healing, defense against pathogens, immune tolerance, allergy, anaphylaxis, autoimmune defects, inflammation, and infectious and other disorders. In the liver, MCs are mainly associated with connective tissue located in the surrounding of the hepatic arteries, veins, and bile ducts. Recent work has demonstrated a significant increase in MC number during hepatic injury, suggesting an important role of these cells in liver disease and progression. In the present review, we summarize aspects of MC function and mediators in experimental liver injury, their interaction with other hepatic cell types, and their contribution to the pathogenesis of fibrosis.
Highlights
Mast Cell DevelopmentMast cells (MCs) are hematopoietic cells of the myeloid lineage [1]. They can be found in tissues with close contact to the environment, such as skin, gastrointestinal tract, upper airways, and lung [2]
Mast cells (MCs) increase constantly over the period peeking in number at week revealed that myofibroblasts and macrophages increase in number during the first ten weeks, whereas
Isolated rat hepatic stellate cells (HSCs) were treated with chymase and it was shown that the proliferation and expression of α-smooth muscle actin and TGF-β1 protein were significantly enhanced in a dose-dependent manner
Summary
Mast cells (MCs) are hematopoietic cells of the myeloid lineage [1]. They can be found in tissues with close contact to the environment, such as skin, gastrointestinal tract, upper airways, and lung [2]. MCs are located in other vascularized organs (e.g., liver and kidney [3,4]) Correlating with their presence in various locations, MCs present as a highly heterogeneous cell population with subtype-dependent differences in cell morphology, histochemical properties, expression of granular proteases, and function, amongst others [5]. This intriguing plasticity and heterogeneity have their origin in the differentiation process of MCs [6]. By applying two different fate mapping mouse models, they could demonstrate that most CTMCs even derive from late erythro-myeloid progenitors generated at the hemogenic endothelium of the yolk sac
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