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On the TRAIL of asthma treatment

In 80% of cases of all cases, asthma attacks are triggered by viruses. Yet, they can also be triggered by allergens such as dust mites, pollen, fungal spores and pet dander. Inhaling these substances brings on the asthma symptoms associated with allergic asthma.
The airways become hypersensitive to the allergens and as a consequence, they are flooded with mucus and the muscles around them tighten. The immune system also overreacts with the invasion of eosinophils and overproduction of IgE creating a chronic state of inflammation. It is generally thought that T helper type 2 (Th2) cells are responsible for the initiation, progression and persistence of the disease because of the panel of cytokines which are secreted and capable of mediating this inflammatory network. Fortunately, not all individuals develop allergies upon exposure to allergens. Some patients just become immune to it following chronic exposure. In their publication in Mucosal Immunology, Dr. Faustino and colleagues from the Department of Immunology at the University of Sao Paulo tried to shed some light on this phenomenon and address some preconceived ideas. Using a well-characterized murine model sensitized to ovalbumin (OVA) to study the effects of chronic intranasal allergen challenges, they demonstrated that the reduction of allergic inflammation was restricted to the lung following long-term allergen challenges. Various studies that based their results on such a model saw a direct correlation between this resolution and the presence of regulatory T (Treg) cells, regulatory B cells and TGF-β1-expressing macrophages. However, they never really looked at the contribution of each one of these populations in the regulation of the immune response. Faustino et al. determined that a positive response to chronic exposure was not due to the presence of Treg cells and associated suppressive cytokines but was rather a consequence of the death by apoptosis of leukocytes. Apoptosis has a critical role in the maintenance of homeostasis and its inhibition was shown to restore allergic airway inflammation. Using an anti-TRAIL blocking antibody, they demonstrated that the TRAIL pathway of apoptosis was associated with the resolution of allergic lung inflammation and that treatment with Enzo’s SuperKillerTRAIL following acute OVA exposure significantly reduced the number of inflammatory cells (both Th2 cells and eosinophils). The authors suggest that TRAIL-mediated apoptosis is key in the attenuation of allergic airway inflammation and could have a huge impact on patients suffering from allergic asthma.

Enzo Life Sciences offers immunologists a comprehensive portfolio for studying the body’s immune response to allergen exposure, including antibodies, detection assays, ELISA kits, and recombinant proteins, some of which are described below:

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References:

  • L. Faustino., et al. Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation. Mucosal Immunol. (2014)..

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