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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mast cell in tissues represents an effector cell capable of elaboration of all the essential mediators of inflammation. The effects of uncontrolled activation may be divided into pharmacologic and inflammatory phases with attendant implications for the initiation of both acute and subacute pathologic processes. The elaboration of chemical mediators by the mast cell makes it possible to recruit blood cells and proteins essential to host defense by a controlled physiologic process that can proceed without significant local tissue damage. When uncontrolled, the same potentiality can be injurious, with the nature of the clinical problem depending upon the location of the cells, the intensity of activation, and the ratio of newly generated and preformed mediators released. The evidence that the mast cell can participate in each form of immunologic reaction--immediate, immune complex, and delayed- as a primary or secondary effector cell and the diversity of its products foretell an evolving recognition of its role in host defense and tissue injury. It is pertinent to develop further methods and criteria to define the nature and extent of mast cell participation in disease processes.
J Invest Dermatol 1976 Sep
PMID:The diversity of mast cell-derived mediators: implications for acute, subacute, and chronic cutaneous inflammatory disorders. 6 Dec 46

This review demonstrates that basophils reflect skin and lung mast cell reactivity and show characteristic changes in mediator release associated with clinical disease. Although the numbers of IgE molecules and IgE receptors on basophils have been enumerated, these have, in most instances, little influence on the release of histamine after challenge. There is, rather, a parameter of "releasability" that may be a major variable in allergic disease states. Basophils contain and release histamine, the eosinophil chemotactic factor of anaphylaxis (ECFA), a slow reacting substance of anaphylaxis (SRS-A), and a kallikrein. The release process is controlled by hormone-basophil receptor interactions that determine the cyclic AMP level; plasma and tissue adenosine levels appear prominent in this control. Histamine feeds back to negatively modulate basophil and mast cell release through a specific histamine 2-receptor; it also inhibits lymphocyte and neutrophil function. Like neutrophils, basophils contain beta-glucuronidase while neutrophils contain SRS-A and a low-molecular-weight ECF. The stimuli for primary basophil and neutrophil release are, however, quite different, although phagocytic stimuli, which fail to cause basophil mediator release, potentiate the IgE response. It is concluded that basophols play a significant in vivo role in inflammation by acting as an interface between foreign antigens, the serum cascade systems, and other inflammatory cells.
J Invest Dermatol 1978 Jul
PMID:The role of basophils in inflammatory reactions. 7 20

The sera of 4 patients with bullous pemphigoid, of 5 patients with drug reactions and of 13 patients with atopic eczema were examined for the occurrence of low molecular weight eosinophil chemotactic factor (ECF) by fractionation on a Sephadex G 25 column. Almost all patients had a peripheral eosinophilia, and many had raised total serum IgE levels. ECF was demonstrated in the sera of all 4 patients with bullous pemphigoid and in 4 of 5 patients with systemic drug reactions. In contrast, the sera of the 13 patients with atopic eczema did not contain any ECF activity, nor did the 13 control sera. These findings suggest that the ECF from phagocytosing polymorphonuclear leukocytes (PMN) and/or the mast cell derived ECF-A contribute to the elevated serum ECF levels in patients with bullous pemphigoid and drug reactions. A correlation between serum ECF and IgE levels and peripheral eosinophilia could not be established.
J Invest Dermatol 1979 Aug
PMID:Serum eosinophil chemotactic factor levels in patients with bullous pemphigoid, drug reactions and atopic eczema. 15 67

Specific antiserum against the purified rat skin main neutral protease was used in double layer immunofluorescent method to localize the enzyme in normal rat skin. The specific immunofluorescence was seen in dermal cells that were identified as mast cells on basis of their metachromatic granules. Enzyme histochemical staining with naphthol AS-D chloroacetate localized to the same cells that exhibited specific immunofluorescence. The granules of isolated rat mast cells also gave a specific reaction with the immunohistochemical technique. The results provide further evidence for the suggestion that rat skin main neutral protease is identical with the rat mast cell "chymase."
J Invest Dermatol 1978 Nov
PMID:Rat skin main neutral protease: immunohistochemical localization. 36 95

Mast cell population density was determined in normal skin from two regions of the arm of several healthy men and compared with blood vessel density and histamine concentration in the same sites. Mast cell and blood vessel counts were made in 1--1.5 micrometer thick plastic sections, by light microscopy and tissue-histamine concentrations were determined by automated fluorimetric analysis. Statistically significant correlations were found between mast cell counts, blood vessel counts and histamine content in skin from the upper arm but no similar correlations were obtained in the forearm. Anatomical differences between the two sites may have been the cause of this discrepancy. Wide variations in mast cell counts and blood vessel density were found in different sections from the same biopsy samples which confirms the notion that dermal mast cells are unevenly distributed. Analysis of variance of the mast cell counts showed that the variance between sections from different blocks from the same biopsy samples was greater than the variance between adjacent biopsies. There was also a marked variation in the histamine content between biopsy samples from sites only 2 cm apart in the same subject.
Br J Dermatol 1979 Jun
PMID:Mast cell population density, blood vessel density and histamine content in normal human skin. 46 10

A new method was developed to define the distribution of mast cells in normal human skin. The population density was determined in a number of zones of different depth in the dermis. Two regions of the same limb were studied systematically. Both were shown to have mast cell populations of similar size and distribution, with a maximum density immediately below the dermo-epidermal junction, gradually falling to a minimum density in the deeper layers of the dermis. Small secondary peaks were less clearly defined at the base of the dermis. These findings should provide baseline data for comparisons with mast cell population size and distribution in different areas of normal skin, or in similar areas in clinical disorders or experimental conditions.
Br J Dermatol 1979 Jun
PMID:Distribution of mast cells in human dermis: development of a mapping technique. 46 11

Granulation tissues, hypertrophic scars, hypertrophic scars treated with mechanical pressure and mature scars from deep thermal injuries, or equivalent trauma, were examined for the presence and dermal distribution of mast cells. Statistical analyses of mast cell counts indicate that 1) the hypertrophic scar contains significantly greater numbers of mast cells than the other tissues studied. 2) as granulation tissue develops interstitial collagen, mast cells begin to appear, 3) mature scars contain significantly fewer mast cells than hypertrophic scars, 4) based on mast cell data, the effect of pressure therapy is first detected in the upper and middle reticularis of the dermis, and 5) on a mast cell statistical basis mature scar and hypertrophic scar under pressure are indistinguishable.
J Invest Dermatol 1978 Jun
PMID:Mast cell analyses in hypertrophic scars, hypertrophic scars treated with pressure and mature scars. 64 83

Co-workers and I examined the early events in the interaction of rat peritoneal mast cells with a number of noncytotoxic mast cell stimuli. These studies demonstrated that an interaction limited to the cytoplasmic membrane is sufficient to induce a secretory mast cell response. Additional experiments suggested that a continued interaction between the stimulus and the membrane receptor is required for maintenance of the secretory response. We have provided evidence to support the concept that different mast cell activators interact with different receptors on the cell membrane and initiate distinct biochemical pathways leading to secretion. Finally, we have shown that pretreatment of mast cells with concentrations of a stimulus that, by themselves, are incapable of initiating a secretory response can profoundly affect the ability of mast cells to respond fully to a subsequent challenge with an optional concentration of stimulus.
J Invest Dermatol 1978 Jul
PMID:Receptor modulation and mast cell secretion. 68 76

Cutaneous necrotizing angiitis may be present as either palpable purpura or less commonly as recurrent urticaria, and each clinical presentation may be associated with hypocomplementemia or a normal complement system. A variety of mechanisms may be operative in the production of necrotic vascular skin lesions that appear as similar, recognizable morphologic lesions. These mechanisms include immune complexes, cellular-type hypersensitivity reactions, and initiation or modulation by mast cells. Two cellular patterns have been recognized in the skin of patients with cutaneous necrotizing angiitis that can be correlated with the involvement of the complement system in serum. In patients with hypocomplementemia, there is an infiltrate of neutrophils that is consistent with a process involving immune complexes; in patients with normocomplementemia there are lymphocytes and activated lymphocytes consistent with participation in part by cellular mechanisms. In both the hypocomplementemic and normocomplementemic forms and as well as in a unique patient in whom the mast cell may initiate the venular damage, the mast cell, which its content of chemical mediators, has the capacity to initiate as well as modulate subacute and chronic vascular damage.
J Invest Dermatol 1976 Sep
PMID:Clinical presentations and mechanisms of necrotizing angitis of the skin. 78 31

Tissue from 134 patients with neurodermatitis and prurigo, pseudoepitheliomatous hyperplasia, pemphigus, and urticaria pigmentosa was examined qualitatively for epidermal mast cells. Epidermal mast cells were found in all of the diseases that were studied except dermatitis herpetiformis. Pemphigus vegetans and dermatitis vegetans were frequently associated with the presence of epidermal mast cells. In other pseudoepitheliomatous diseases, such as tuberculosis verrucosa cutis, blastomycosis, and bromoderma, epidermal mast cells were present in many cases. Four of eight patients with acral dermatitis with elevated IgE blood levels had intraepidermal mast cells; the number was much lower in patients with usual neurodermatitis and prurigo nodularis. Only two of ten cases of alopecia mucinosa showed epidermal mast cells. A single epidermal mast cell was found in ten cases of urticaria pigmentosa. Chronic inflammation associated with epidermal cell proliferation appeared to correlate with the presence of epidermal mast cell.
Arch Dermatol 1977 Feb
PMID:Epidermal mast cells. 83 93


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