The human mast cell☆☆☆★

Church, Martin K.; Levi‐Schaffer, Francesca

doi:10.1016/s0091-6749(97)70089-7

Cited by 313 publications

(203 citation statements)

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“…It is now clear that this view was too limited as we have begun to appreciate the function of mast cells in innate immunity and a possible role in autoimmune disease [8,9]. Mast cels are multifunctional, tissue-dwelling cells [20] and a potential source of proinflammatory cytokines and chemotactic mediators [21] which are decisive in initiating the immune and inflammatory responses. Despite the fact that IgE/Ag binding to mast cells is the primary stimulus for activating mast cell degranulation and cytokine production, it is clear that IgE-independent stimuli can activate these cells and induce inflammation [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress stimulates IL‐4 and IL‐6 production in mast cells by an APE/Ref‐1‐dependent pathway

Frossi

Carli

Daniël³

et al. 2003

Eur J Immunol

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Section: Discussionmentioning

confidence: 99%

Oxidative stress stimulates IL‐4 and IL‐6 production in mast cells by an APE/Ref‐1‐dependent pathway

Frossi

Carli

Daniël³

et al. 2003

Eur J Immunol

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“…In another study fatal asthma was characterized by an increase in both numbers of large vessels and total vessel area in the cartilaginous airways, suggesting enlargement of existing vessels [6]. The authors have not assessed large airway vessel size and area, because such measurements may be artificially distorted by tangential cutting of vessels and vasodilatation induced by b 2 -agonists [19] or vasoactive mediators [20]. Furthermore, results from animal studies have shown that most of the airway narrowing is due to extravasation of plasma fluid rather than vascular congestion [21].…”

Section: Discussionmentioning

confidence: 99%

“…However, the increase in the numbers of mucosal vessels may in itself have two important pathophysiological consequences for the persistent airflow obstruction frequently observed in severe asthmatic patients. First, it is possible that bronchial vasocongestion and microvascular leakage induced by leukotriene and histamine may lead to transient increases in airway wall thickness [20]. Second, the abundant vascularity and associated ICAM-1 expression may enhance sequestration and adhesion of inflammatory cells [7,22].…”

Section: Discussionmentioning

confidence: 99%

Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Vrugt¹,

Wilson²,

Bron³

et al. 2000

Eur Respir J

131

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To examine the role of the bronchial microvasculature and adhesion molecule expression in severe asthma, the authors have performed an immunohistochemical study on bronchial biopsies comparing 15 glucocorticoid-dependent asthmatics, 15 mild asthmatics and eight control subjects.Serially cut glycol methacrylate-embedded sections were stained with monoclonal antibodies identifying the vessel marker EN-4, intercellular adhesion molecule (I-CAM)-1, vascular cell adhesion molecule (VCAM)-1, E-and P-selectin. Sections were also stained for lymphocyte function associated antigen (LFA)-1 and very late antigen (VLA)-4.By comparison with mild asthma and nonasthma, severe asthma was characterized by increased numbers of submucosal vessels (p=0.009) which was associated with increased numbers of vessels expressing ICAM-1 (p=0.005). A highly significant correlation was found between the total number of EN-4+ vessels and the vessels expressing ICAM-1 (r=0.85, p=0.01). In contrast, E-selectin expression was lower in severe as compared with mild asthma (p=0.01) but not different from normal. No differences were found between the three groups in the expression of VCAM-1 and Pselectin nor in numbers of LFA-1+ and VLA-4+ cells.The results of this study support the notion that mucosal neovascularization is an important feature of airways remodelling in severe asthma. This is associated with a relatively higher density of vessels expressing intercellular adhesion molecule-1, although the expression of this adhesion molecule per vessel was not raised.

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“…[15][16][17] Mast cells originate from the bone marrow and the immature progenitor cells migrate to peripheral tissues and mature in situ. [18][19][20] Mast cells are not identified in the circulation. 21 Mast cells possess many properties that enable them to participate in a diverse range of biological activities.…”

mentioning

confidence: 99%

Mast cells and cutaneous malignancies

Ch’ng

Wallis

Yuan³

et al. 2006

Modern Pathology

168

166

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This paper reviews the role of mast cells in the development and progression of basal cell carcinoma, squamous cell carcinoma and malignant melanoma. Mast cells accumulate around cutaneous malignancies. Current evidence suggests that mast cells contribute to the tumorigenesis of cutaneous malignancies through four mechanisms. (1) Immunosuppression: Ultraviolet-B radiation, the most important initiator of cutaneous malignancies, activates mast cells. Upon irradiation of the skin, trans-urocanic acid in the epidermis isomerizes to cis-urocanic acid, which stimulates neuropeptide release from neural c-fibers. These neuropeptides in turn trigger histamine secretion from mast cells, leading to suppression of the cellular immune system. (2) Angiogenesis: Mast cells are the major source of vascular endothelial growth factor in basal cell carcinoma and malignant melanoma. Vascular endothelial growth factor is one of the most potent angiogenic factors, which also induces leakage of other angiogenic factors across the endothelial cell wall into the matrix. Mast cell proteases reorganize the stroma to facilitate endothelial cell migration. As well, heparin, the dominant mast cell proteoglycan, assists in blood-borne metastasis. (3) Degradation of extracellular matrix: Through its own proteases, and indirectly via interaction with other cells, mast cells participate in degradation of the matrix, which is required for tumor spread. (4) Mitogenesis: Mast cell mediators including fibroblast growth factor-2 and interleukin-8 are mitogenic to melanoma cells. Current evidence supports an accessory role for mast cells in the development and progression of cutaneous malignancies. Emerging data, however, also suggest that mast cells might, in fact, have opposing roles in tumor biology, and the microenvironment could polarize mast cells to possess either promoting or inhibitory effects on tumors.

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The human mast cell☆☆☆★

Cited by 313 publications

References 0 publications

Oxidative stress stimulates IL‐4 and IL‐6 production in mast cells by an APE/Ref‐1‐dependent pathway

Oxidative stress stimulates IL‐4 and IL‐6 production in mast cells by an APE/Ref‐1‐dependent pathway

Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Mast cells and cutaneous malignancies

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