Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In previous studies basophil-bound IgE was measured by means of quantitative immunofluorescence miscroscopy. But mast cells are of particular importance in local atopic reactions, we thought it necessary to investigate the IgE-load on both cell types. The amount of mast cell-bound IgE can be estimated in a semiquantitative way by end point titration with a fluoresceinated sheep antihuman IgE (FlaIgE). The amount of mast cell-bound IgE was estimated this way in tonsils, adenoids, bronchial and tracheal tissues, and was compared with the amount of IgE on the basophils. A correlation was found between the IgE-load on mast cells and on basophils. Atopic patients had a higher mast cell fluorescence titer (MCFT) than nonatopic controls. It was demonstrated that, as on basophils, the IgE level of the serum contributes to this difference.
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PMID:Cell-bound IgE on human mast cells and basophilic granulocytes in atopic and nonatopic subjects. 32 9

Human mast cells likely play a significant role in human asthma. In the present study, concentrations of tryptase and histamine in bronchoalveolar lavage fluid (BALF) were used as indicators of pulmonary mast cell activation. BALF was obtained before and after endobronchial allergen challenge and assessed for mediator content and cell composition in 4 subject groups: nonatopic nonasthmatics (Group 1, n = 7), nonatopic asthmatics (Group 2, n = 3), atopic nonasthmatics (Group 3, n = 7), and atopic asthmatics (Group 4, n = 7). Before challenge, histamine concentrations were not different between the 4 groups, whereas tryptase concentrations were significantly greater in the atopic asthmatics than in each of the other groups (p less than 0.04). Allergen challenge in atopic asthmatics resulted in significant increases above baseline in mean +/- SD histamine (0.7 +/- 7.1 to 2.8 +/- 2.0 ng/ml) and tryptase (2.0 +/- 1.7 to 10.1 +/- 8.2 ng/ml) concentrations in BALF (p less than 0.03). Atopic nonasthmatics also had increases above baseline in histamine (0.2 +/- 0.2 to 1.2 +/- 1.4 ng/ml) and tryptase (0.5 +/- 0.4 to 1.4 +/- 1.03 ng/ml) concentrations after allergen challenge (p less than 0.05). Though the histamine values were not significantly different between atopic nonasthmatics and atopic asthmatics after allergen challenge, tryptase concentrations were markedly higher in the atopic asthmatic group. The numbers, as well as the predominance of the T mast cell type in atopic asthmatics and nonasthmatics, were no different from controls. In nonatopic subjects, regardless of asthmatic state, histamine or tryptase concentrations were not altered by allergen challenge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of pulmonary mast cells by bronchoalveolar allergen challenge. In vivo release of histamine and tryptase in atopic subjects with and without asthma. 246 67

Isolated dermal mast cells from atopic dogs are a valuable tool for the analysis of their functional properties in atopic dermatitis. We have characterized the histamine secretory pattern of mast cells enzymatically dispersed from the skin of dogs naturally suffering from this condition. The total histamine content found per isolated skin mast cell was higher in the allergic dogs than in nonatopic (control) animals (8.7 pg/mast cell versus 5.2 pg/mast cell). This phenomenon together with the well known higher concentration of skin mast cell number in atopic dermatitis lesions might account for the observed increase in local histamine concentration (15.0 micrograms/g versus 9.0 micrograms/g). Atopic dog-derived mast cells were highly reactive to both non-immunological (ionophore A23187) and an immunological-like (concanavalin A) stimulus. Furthermore, histamine net release induced by concanavalin A (1 mg/ml) stimulation was clearly enhanced in the atopic dogs (33.3% net release versus 15.4% in controls). These results have not been described in dermal mast cells dispersed from the skin of individuals with atopic dermatitis and clearly support the hypothesis that mast cells play a major role in causing and possibly modulating atopic dermatitis, through enhanced sensitivity or releasability. However, whether these two phenomena are primary abnormalities of atopic dermatitis, or only secondary changes, remains undetermined.
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PMID:Skin mast cell releasability in dogs with atopic dermatitis. 887 17

Some individuals question whether any treatment is effective in severe alopecia areata. Certainly many patients, especially those with mild disease, experience spontaneous hair regrowth; however, results of double-blind studies clearly indicate that some treatments do promote hair regrowth even in those with extensive disease. Some patients never show either spontaneous or treatment-related hair regrowth; others experience hair regrowth only while maintained on treatment, repeatedly losing hair within a few weeks of discontinuing treatment and regrowing it within several weeks after restarting treatment. Some patients who have been responsive to treatment may experience exacerbation of their disease such that even high-dose systemic steroids do not prevent the development of alopecia universalis. Some treatments appear to work on some patients some or all of the time, but no treatment appears to work on all patients all of the time. We would suggest a few practical points that we find useful: To maximize the potential for cosmetic hair growth in alopecia areata that is extensive or flaring, treat the entire scalp instead of "chasing" patches. Do not change any topical treatment sooner than 3 months after starting it; early regrowth may first be present at 3 months. Cosmetic regrowth may take a year or more to achieve. Maintenance treatment increases the likelihood of maintenance of cosmetic hair growth, but patches of hair loss may still come and go. Atopic patients who experience seasonal hair loss may benefit (ie, have less severe hair loss flares or respond more readily to topical therapy) by using an antihistamine or mast cell stabilizer prophylactically. Whether one looks at the therapeutic cup as half full or half empty, most patients urge us to continue to try to find safe, effective long-term treatments for this disease.
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PMID:Treatment of alopecia areata. 923 31

Stem cell factor (SCF) influences mast cell activation and inflammatory mediator release, and is elevated in tissues undergoing allergic inflammation. Wheal formation in response to the injection of SCF or anti-immunoglobulin (Ig)E antibody injection was compared between normal (n = 10) and nonlesional atopic (n = 10) canine skin. In situ SCF secretion was compared between lesional and nonlesional skin using immunohistochemistry. Histamine release by skin cell suspensions after stimulation with SCF, concanavalin A (ConA) or rabbit anticanine IgE antibodies was compared between normal and atopic dogs. All dogs exhibited strong responses to intradermal SCF injection at 10 and 50 ng mL(-1). Atopic dogs had significantly (P = 0.002) larger wheal responses to anti-IgE than normal dogs; but there was no difference in numbers of skin mast cells bearing IgE as detected by immunohistochemistry. Only atopic dogs exhibited interstitial deposition of SCF in both lesional and nonlesional skin specimens. Median histamine release stimulated by SCF in the absence of IgE from lesional skin cells was higher in atopic than normal dogs (P = 0.04). These experiments suggest that dermal SCF secretion could potentiate histamine release following IgE receptor cross-linking and thus, could be one of the explanations for the inherent mast cell hyperexcitability observed in canine atopic dermatitis.
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PMID:Skin mast cell histamine release following stem cell factor and high-affinity immunoglobulin E receptor cross-linking in dogs with atopic dermatitis. 1184 24

Atopic ocular diseases involve a spectrum of immuno-inflammatory responses. There are minimal pathologic changes with SAC. With PAC, there is increased mast cell activation and late-phase inflammatory cell infiltrate as a consequence of continued allergic stimulation. Associated with the more chronic and severe forms of atopic ocular disorders, GPC, VKC and AKC, there is persistent mast cell, eosinophil, and lymphocyte activation resulting in pathologic changes. Therapeutic intervention for atopic ocular diseases has focused on symptomatic improvement. However, with an increasing understanding of the molecular mechanisms associated with the allergic inflammatory response, experimental studies may facilitate the development of preventative strategies.
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PMID:Atopic ocular disease. 1206 72

Atopic allergies have increased during the past 20-30 years in frequency quite dramatically and in many countries have reached almost epidemic proportions. Allergies have thereby become one of the major medical issues of the western world. Immunoglobulin E (IgE) is here a central player. IgE is the Ig class that is present in the lowest concentration in human plasma. IgG is, for example, 10 000 to 1 million times more abundant than IgE. However, despite of its low plasma levels IgE is a very important inducer of inflammation, due to its interaction with high-affinity receptors on mast cell and basophils. IgE has been conserved as a single active gene in all placental mammals studied, and the expression of this gene is under a very stringent control, most likely due to its very potent inflammatory characteristics. IgE expression is being regulated at many levels: by cytokines, switch region length, positive and negatively acting transcription factors and suppressors of cytokine signaling (SOCS). In addition, the plasma half-life differs markedly for IgG and IgE, with 21 and 2.5 days, respectively. This review summarizes the rapid progress in our understanding of the complex network of regulatory mechanisms acting on IgE and also how this new information may help us in our efforts to control IgE-mediated inflammatory conditions.
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PMID:Regulation of IgE homeostasis, and the identification of potential targets for therapeutic intervention. 1714 60

Drug allergy is a rising problem in the twenty-first century which affects all populations and races, children, and adults, and for which the recognition, diagnosis, management, and treatment is still not well standardized. Classical and new chemotherapy drugs, monoclonal antibodies (MoAbs), and small molecules to treat cancer and chronic inflammatory diseases are aimed at improving quality of life and life expectancy of patients, but an increasing number of reactions including anaphylaxis precludes their use in targeted populations. Women are more affected by drug allergy and up to 27% of women with ovarian and breast cancer develop carboplatin allergy after multiple cycles of treatment. Carriers of BRCA genes develop drug allergy after fewer exposures and can present with severe reactions, including anaphylaxis. Atopic patients are at increased risk for chemotherapy and MoAbs drug allergy and the current patterns of treatment with recurrent and intermittent drug exposures may favor the development of drug allergies. To overcome drug allergy, desensitization has been developed, a novel approach which provides a unique opportunity to protect against anaphylaxis and to improve clinical outcomes. There is evidence that inhibitory mechanisms blocking IgE/antigen mast cell activation are active during desensitization, enhancing safety. Whether desensitization modulates drug allergic and anaphylactic responses facilitating tolerance is currently being investigated. This review provides insight into the current knowledge of drug allergy and anaphylaxis to cancer and chronic inflammatory diseases drugs, the mechanisms of drug desensitization and its applications to personalized medicine.
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PMID:Drug Hypersensitivity and Anaphylaxis in Cancer and Chronic Inflammatory Diseases: The Role of Desensitizations. 2916 36