Gurish MF, Boyce JAMast cells: ontogeny, homing, and recruitment of a unique innate effector cell. J Allergy Clin Immun 117:1285-1291

Harvard University, Cambridge, Massachusetts, United States
Journal of Allergy and Clinical Immunology (Impact Factor: 11.25). 07/2006; 117(6):1285-91. DOI: 10.1016/j.jaci.2006.04.017
Source: PubMed

ABSTRACT Mast cells (MCs) are found principally in peripheral tissues yet are of bone marrow origin. Recent studies in mice trace the MC lineage from the common myeloid progenitor through the granulocyte-macrophage progenitor in the bone marrow to a committed MC progenitor (MCP). Additionally, at least in the mouse, a bipotent basophil-MC progenitor has been identified in the spleen, suggesting a physiologic role for this organ in MC development. MCPs are especially abundant in the mouse intestine, likely ensuring the capacity for a rapid expansion of MCs in the intestinal epithelium during the effector response to helminth infection and perhaps providing a pool of committed cells capable of redistribution to other tissues. Migration of MCPs to the intestine is constitutive and controlled by alpha chemokine receptor 2 and alpha4beta7 integrins expressed on the MCPs, with the latter integrin interacting with endothelial vascular cell adhesion molecule 1 and mucosal addressin cell adhesion molecule 1. In contrast, normal mouse lung tissue contains few MCPs and MCs, and these cellular reservoirs are not affected by the lack of alpha chemokine receptor 2 or alpha4beta7 integrin. Nonetheless, robust recruitment of MCPs to the lung occurs during experimentally induced allergic pulmonary inflammation and requires alpha4beta7 and alpha4beta1 integrins interacting with vascular cell adhesion molecule 1 but not with mucosal addressin cell adhesion molecule 1. Thus although MCs are present in all organs, the pathways responsible for the trafficking of MCPs from the circulation are organ specific and include both constitutive and inducible systems, ensuring both resident MCs and the potential for incremental recruitment in accord with the requirements of the immune response. These findings in mice await confirmation in human subjects.

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    • ". SCF participates in each stage of growth and differentiation of MCs including differentiation, proliferation, chemotaxis, adhesion, and survival [81]. It has been suggested that this global influence of SCF results in the ubiquitous presence of MCs [82]. There are numerous growth and differentiation factors other than SCF, which have been shown to affect MC functions including several of the type 2 helper T cell cytokines [83]. "
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    ABSTRACT: Despite years of intensive investigation that has been made in understanding prostate cancer, it remains one of the major men's health issues and the leading cause of death worldwide. It is now ascertained that prostate cancer emerges from multiple spontaneous and/or inherited alterations that induce changes in expression patterns of genes and proteins that function in complex networks controlling critical cellular events. It is now accepted that several innate and adaptive immune cells, including T- and B-lymphocytes, macrophages, natural killer cells, dendritic cells, neutrophils, eosinophils, and mast cells (MCs), infiltrate the prostate cancer. All of these cells are irregularly scattered within the tumor and loaded with an assorted array of cytokines, chemokines, and inflammatory and cytotoxic mediators. This complex framework reflects the diversity in tumor biology and tumor-host interactions. MCs are well-established effector cells in Immunoglobulin-E (Ig-E) associated immune responses and potent effector cells of the innate immune system; however, their clinical significance in prostate cancer is still debated. Here, these controversies are summarized, focusing on the implications of these findings in understanding the roles of MCs in primary prostate cancer.
    Disease markers 11/2013; 35(6):711-720. DOI:10.1155/2013/478303 · 2.17 Impact Factor
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    • "A milestone in our understanding of the biological profile of tissue MCs was the discovery that these cells originate from haematopoietic stem cells in the bone marrow, foetal liver, and cord blood. These progenitor cells circulate in the blood as non-granulated committed precursors [16] [17] [18]. Precursor cells migrate into different tissues in which they proliferate and differentiate into mature, granulated cells under the influence of several microenvironmental growth factors, in particular stem cell factor (SCF), the ligand for the c-kit tyrosine kinase III growth factor receptor (CD117) – secreted by fibroblasts, stromal cells and endothelial cells – which critically regulates many aspects of MC development and survival [19] [20]. "
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    ABSTRACT: Accumulation of mast cells (MCs) in tumours was described by Ehrlich in his doctoral thesis. Since this early account, ample evidence has been provided highlighting participation of MCs to the inflammatory reaction that occurs in many clinical and experimental tumour settings. MCs are bone marrow-derived tissue-homing leukocytes that are endowed with a panoply of releasable mediators and surface receptors. These cells actively take part to innate and acquired immune reactions as well as to a series of fundamental functions such as angiogenesis, tissue repair, and tissue remodelling. The involvement of MCs in tumour development is debated. Although some evidence suggests that MCs can promote tumourigenesis and tumour progression, there are some clinical sets as well as experimental tumour models in which MCs seem to have functions that favour the host. One of the major issues linking MCs to cancer is the ability of these cells to release potent pro-angiogenic factors. This review will focus on the most recent acquisitions about this intriguing field of research. This article is part of a Special Issue entitled: Mast cells in inflammation.
    Biochimica et Biophysica Acta 12/2010; 1822(1):2-8. DOI:10.1016/j.bbadis.2010.11.010 · 4.66 Impact Factor
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    • "Committed mast cell progenitors reside at special anatomical sites (for example, intestine and hair follicles) and locally proliferate with terminal maturation (Kumamoto et al., 2003; Gurish and Boyce, 2006). Proliferation, terminal differentiation, and survival of resident mast cells require growth factors, such as IL-3, stem cell factor, and/or other factors (Gurish and Boyce, 2006). At least two types of mast cells have been historically identified in rodents based on their morphological, biochemical, and functional properties (Kitamura, 1989). "
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    ABSTRACT: Mast cells are widely distributed throughout the body, being preferentially localized at host-environment interfaces. They have long been known as major effector cells in IgE-mediated allergic responses. However, accumulating evidence has provided many new insights into their functions. They are now known to be involved in diverse pathological processes, for example, innate and adaptive immunity. Utility of mast cell-deficient mice and mast cell-knock-in mice has provided powerful models to demonstrate compelling evidence for their in vivo relevance. Conversely, primary cultures of tissue-derived mast cells provide excellent models for in vitro studies of functions at both cellular and molecular levels. Because mast cells exhibit phenotypical and functional heterogeneity in different anatomical sites, it is important to obtain tissue-specific mast cells to clarify their function in tissue. In this regard, researchers have established several methods to prepare mast cells from different tissues, which are technically difficult to obtain at high purity and yield. To overcome these difficulties, we have developed a primary culture system to obtain large numbers of mast cells at high purity from murine fetal skin. In this review, we describe characteristics of such mast cells and their utility in mast cell biology.
    Journal of Investigative Dermatology 03/2009; 129(5):1120-5. DOI:10.1038/jid.2009.44 · 6.37 Impact Factor
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