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hypersensitivity/protease

Врската е зачувана во таблата со исечоци
Страница 1 од 1739 резултати

Allergic reactions, including asthma, to the pineapple protease bromelain following occupational exposure.

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A 58-year-old pharmaceutical worker regularly developed asthma and rhinitis when handling bromelain, a purified protease of pineapple (Ananas comosus), at her work-place, where she had been employed for about 10 years. RAST and prick test showed strong positive reactions to bromelain. Both

Barrier dysfunction caused by environmental proteases in the pathogenesis of allergic diseases.

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Skin barrier dysfunction has emerged as a critical driving force in the initiation and exacerbation of atopic dermatitis and the "atopic march" in allergic diseases. The genetically determined barrier deficiency and barrier disruption by environmental and endogenous proteases in skin and epithelium

Role of cockroach proteases in allergic disease.

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Allergic asthma is on the rise in developed countries, and cockroach exposure is a major risk factor for the development of asthma. In recent years, a number of studies have investigated the importance of allergen-associated proteases in modulating allergic airway inflammation. Many of the studies

The role of protease activation of inflammation in allergic respiratory diseases.

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Extracellular endogenous proteases, as well as exogenous proteases from mites and molds, react with cell-surface receptors in the airways to generate leukocyte infiltration and to amplify the response to allergens. Stimulation leads to increased intracellular Ca ++ and gene transcription. The most

A protease-activated pathway underlying Th cell type 2 activation and allergic lung disease.

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The respiratory allergens that induce experimental Th cell type 2-dependent allergic lung inflammation may be grouped into two functional classes. One class of allergens, in this study termed type I, requires priming with adjuvants remote from the lung to overcome airway tolerogenic mechanisms that

IL-33-mediated innate response and adaptive immune cells contribute to maximum responses of protease allergen-induced allergic airway inflammation.

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How the innate and adaptive immune systems cooperate in the natural history of allergic diseases has been largely unknown. Plant-derived allergen, papain, and mite allergens, Der f 1 and Der p 1, belong to the same family of cysteine proteases. We examined the role of protease allergens in the

Epicutaneous Allergic Sensitization by Cooperation between Allergen Protease Activity and Mechanical Skin Barrier Damage in Mice.

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Allergen sources such as mites, insects, fungi, and pollen contain proteases. Airway exposure to proteases induces allergic airway inflammation and IgE/IgG1 responses via IL-33-dependent mechanisms in mice. We examined the epicutaneous sensitization of mice to a model protease allergen, papain; the

Continued therapy with HIV-1 protease inhibitors, despite previous hypersensitivity reactions, through coadministration of prednisone.

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We describe an HIV-1 positive patient who developed severe hypersensitivity reactions during treatment with each of the three currently available protease inhibitors. Addition of prednisone enabled continued use of saquinavir, one of these protease inhibitors, thereby achieving a degree of viral

Mast cell distribution and neutral protease expression in acute and chronic allergic conjunctivitis.

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Allergic eye disease has a variety of clinical manifestations including seasonal atopic conjunctivitis (SAC), perennial atopic conjunctivitis (PAC), atopic keratoconjunctivitis (AKC), and atopic blepharoconjunctivitis (ABC). We have investigated the number, distribution and protease expression of

Blocking of protease allergens with inhibitors reduces allergic responses in allergic rhinitis and other allergic diseases.

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CONCLUSIONS Allergic responses specific to the corresponding proteases were reduced by protease inhibitors, suggesting promise as potent treatments for allergic rhinitis and other allergic conditions. OBJECTIVE Allergic diseases, such as allergic rhinitis, are caused by the overproduction of IgE

Development of Aspergillus protease with ovalbumin-induced allergic chronic rhinosinusitis model in the mouse.

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BACKGROUND Chronic rhinosinusitis (CRS) is a multifactorial inflammatory disease. Particularly, eosinophilic CRS is often recalcitrant to treatment, so an appropriate animal model is required to evaluate the pathogenesis of, and to develop therapies for, recalcitrant eosinophilic CRS. This study

A high-molecular-weight trypsinlike protease in the skin sites of delayed hypersensitivity in guinea pigs.

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A trypsinlike protease was extracted from the delayed hypersensitivity skin sites in guinea pigs. Extractable amounts of the enzyme were chronologically paralleled with the gross appearance of the inflammation, and the maximum activity from the inflamed sites at 24-36 hours was about 20 times

Isolation of a thiol-dependent serine protease in peanut and investigation of its role in the complement and the allergic reaction.

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A serine protease activity was detected in aqueous peanuts seeds extracts, partially purified and characterized as a thiol-dependent serine protease. The potential role of this proteolytic activity on allergic reaction to peanuts was prospected through complement activation studies in human plasma

A Fungal Protease Model to Interrogate Allergic Lung Immunity.

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Allergic airway diseases (asthma and chronic rhinosinusitis) are among the most common of all human diseases in heavily industrialized societies. Animal models of asthma have provided remarkable insight into allergic disease pathogenesis and will continue to drive the discovery of new therapeutic

MALT1 Protease Plays a Dual Role in the Allergic Response by Acting in Both Mast Cells and Endothelial Cells.

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The signaling protein MALT1 plays a key role in promoting NF-κB activation in Ag-stimulated lymphocytes. In this capacity, MALT1 has two functions, acting as a scaffolding protein and as a substrate-specific protease. MALT1 is also required for NF-κB-dependent induction of proinflammatory cytokines
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