Regulation of mast cell differentiation

Kitamura, Yukihiko; Fujita, Jun

doi:10.1002/bies.950100604

Cited by 34 publications

(26 citation statements)

References 22 publications

(4 reference statements)

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“…Sash Ϫ/Ϫ mice carry a mutation upstream from the white spotting (W) locus causing disruption of the 5Ј regulatory sequences and therefore reduced signaling through c-kit tyrosine kinase (30). This reduced c-kit expression in the bone marrow causes an inability of hematopoietic stem cells to differentiate into mast cell precursors resulting in a complete lack of mast cells (31,72). No other known disruptions in the development of hematopoietic stem cell derivatives or any other irregularities in c-kit receptor mRNA or protein expression, with the exception of melanocytes (causing irregular fur pigmentation), have been found (30).…”

Section: Methodsmentioning

confidence: 99%

Brain mast cells link the immune system to anxiety-like behavior

Nautiyal

Ribeiro

Pfaff

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

160

119

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Section: Methodsmentioning

confidence: 99%

Brain mast cells link the immune system to anxiety-like behavior

Nautiyal

Ribeiro

Pfaff

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

160

119

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“…But how mast cells affect immunosuppressive and inflammatory cells in tumor microenvironment remains largely unclear. SCF and its cognate receptor c-kit on mast cells are crucial for directing mast cell development from their hematopoietic progenitors, influencing numbers and phenotypes of mast cells [45]. Other effectors, such as IL-3, are also involved in mast cell development and survival [45,46].…”

Section: Mast Cells Remodel Tumor Microenvironments Through Interactimentioning

confidence: 99%

Mast cell: insight into remodeling a tumor microenvironment

Liu

Zhang

Zhao

et al. 2011

Cancer Metastasis Rev

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Mast cells are of paramount importance to allergies, pathogen immune responses during infections, and angiogenesis, as well as innate and adaptive immune regulations. Beyond all these roles, mast cells are now more and more being recognized as modulators of tumor microenvironment. Notwithstanding mounting evidences of mast cell accumulation in tumors, their exact role in tumor microenvironment is still incompletely understood. In this review, we discuss the significant role of mast cells in the remodeling of tumor microenvironment by either releasing various factors after activation or interacting with other cells within tumor and, as a result, the possible role of mast cell in cancer invasion and metastasis. We also discuss recent findings that mast cells actively release microparticles, which account for the transfer of membrane-type receptor signal and regulatory molecules such as microRNAs to tumor cells and immune cells. These findings on mast cells provide further insights into the complexity of tumor microenvironment remodeling.

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“…It was initially suggested that they derive from T lymphocytes, fibroblasts, or macrophages [4,5], but the current general consensus suggests that they originate from pluripotent hemapoietic stem cells in bone marrow (BM) [6], whence they are released into the blood as progenitors and only undergo terminal differentation into mature MCs after they have entered tissues (Fig. 1): i.e., they invade connective or mucosal tissue as morphologically unidentifiable MC precursors and differentiate into phenotypically identifiable MCs only at the tissue level [7][8][9][10].…”

Section: The Physiology Of Mast Cellsmentioning

confidence: 99%

The Complex Functions of Mast Cells in Chronic Human Liver Diseases

et al. 2006

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Mast cells (MCs) are multifunctional effector cells of the immune system. MCs were originally thought to be involved in IgE-associated immediate hypersensitivity and allergic disorders, but it is now known that they contain or elaborate an array of mediators with a multitude of effects on many other cells. A number of studies have found that MCs are involved in various liver diseases. Although still controversial, they seem to be involved in the liver's fibrotic response to chronic inflammation and parasitic infection. Hepatic fibrosis is the most frequent liver response to toxic, infectious, or metabolic agents. During the establishment of this pathological condition, there is an increase in the components of the basement membrane that leads to continuous basement membrane-like structures being raised within Disse's space and a decrease in the number of sinusoid endothelial fenestrae. This leads to a complex process called "sinusoidal capillarization." At the cellular level, liver fibrogenesis is initiated by hepatocyte necrosis, which induces the recruitment of a large number of inflammatory cells, including MCs, which can be considered the primary effectors of the process changing sinusoidal endothelial cells into capillary-type endothelial cells. We review the roles played by MCs in hepatic chronic diseases and describe a biopsy section of hepatic tissue taken from a patient with chronic C virus-related hepatitis showing diffuse sinusoidal capillarization and a high density of MCs. This observation has led us to hypothesize a relationship between these highly specialized cells and sinusoidal capillarization.

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Regulation of mast cell differentiation

Cited by 34 publications

References 22 publications

Brain mast cells link the immune system to anxiety-like behavior

Brain mast cells link the immune system to anxiety-like behavior

Mast cell: insight into remodeling a tumor microenvironment

The Complex Functions of Mast Cells in Chronic Human Liver Diseases

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