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)

Atopic dermatitis, a common, chronic, inflammatory skin disease that occurs with increasing prevalence, is characterized by hyperactivated cytokines of helper T cell subset 2 and is frequently associated with staphylococcal infection. An experimental animal model of atopic dermatitis induced by transgenically introduced cytokine is not available. We generated a transgenic mouse line expressing epidermal interleukin-4, a critical cytokine of helper T cell subset 2. Here we show that transgenic mice spontaneously developed a pruritic inflammatory skin disease reproducing all key features of human atopic dermatitis, including xerosis, conjunctivitis, inflammatory skin lesions, Staphylococcus aureus infection, histopathology of chronic dermatitis with T cell, mast cell, macrophage-like mononuclear cell, and eosinophil infiltration, and elevation of total serum IgE and IgG1. The onset and early progression of skin disease coincided with increased total serum IgE and IgG1. The mouse disease occurred at a 43% annual incidence rate and primarily affected the poorly haired skin: ear (100%), neck (65%), eye (53%), face (29%), tail (12%), leg (12%), and torso (6%). As a group the affected transgenic mice manifested with a skin disorder that fulfilled the clinical diagnostic criteria established for atopic dermatitis in human patients. Pending further characterization to authenticate it as a model of atopic dermatitis, this experimental animal model of pruritic inflammatory skin disease may facilitate investigations for the roles of interleukin-4 in cutaneous inflammation and skin infection in human patients.
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PMID:Expression of interleukin-4 in the epidermis of transgenic mice results in a pruritic inflammatory skin disease: an experimental animal model to study atopic dermatitis. 1167 41

Racial (ethnic) differences in skin properties may explain racial disparities seen in dermatologic disorders and provide insight into appropriate differences in the management of these disorders. However, racial differences in skin have been minimally investigated by objective methods and the data are often contradictory. Objective methods studied include transepidermal water loss (TEWL), water content (WC), corneocyte variability, blood vessel reactivity, elastic recovery/extensibility, pH gradient, lipid content, surface microflora, microscopic evaluation of mast cell granules, and confocal microscopy. The majority of the evidence (six out of eight studies) indicates that TEWL is greater in Black skin compared with White skin. TEWL measurements of Asian skin are inconclusive as they have been found to be equal to Black skin and greater than Caucasian skin, equal to Caucasian skin, and less than all other ethnic groups in different studies. Racial differences in WC, as measured by resistance, capacitance, conductance and impedance, are also inconclusive as the data are contradictory. While the evidence regarding corneocyte desquamation is minimal, one clinically provocative observation is that Blacks have a 2.5 times greater spontaneous desquamation rate compared with Caucasians and Asians, possibly accounting for an increased frequency of xerosis seen clinically in Blacks. With regards to blood vessel reactivity, studies can not be compared to each other because each uses different vasoactive substances. However, each study, except for one study comparing Hispanics and Whites, and another comparing Japanese and German women, reveal some degree of racial variation in blood vessel reactivity. It has been demonstrated that the pH of Black skin is less than White skin; however, the studies that have demonstrated this have done so under different skin conditions and on different anatomic sites. Racial differences in lipid content are inconclusive. Additionally, there is insufficient and conflicting evidence to make conclusions regarding racial differences in skin biomechanics and skin microflora. Microscopic evaluation reveals that Black skin contains larger mast cell granules, and differences in stuctural properties and enzymes of mast cells compared with White skin, possibly accounting for differences in pruritus experienced by the individuals of these racial groups. There exists substantial evidence to support that Black skin has a higher TEWL, variable blood vessel reactivity, decreased skin surface pH, and larger mast cell granules compared with White skin. Although some deductions have been made about Asian and Hispanic skin, further evaluation needs to be done. Differences in WC, corneocyte desquamation, elastic recovery/extensibility, lipid content and skin microflora, although statistically significant, are inconclusive.
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PMID:Racial (ethnic) differences in skin properties: the objective data. 1464 Jul 77