Allergic diseases are type 2 inflammatory reactions with an increasing worldwide prevalence, making the search for new therapeutic options pertinent. Allergen immunotherapy is the only disease-modifying approach for allergic rhinitis, though it can result in systemic reactions. Recently, peptide immunotherapy (PIT), involving T cell epitope peptides that bind to major histocompatibility complexes, have been developed. It is speculated that they can induce T helper cell type 2 anergy, Treg cell upregulation or immune deviation. Promising results in cat dander, honeybee venom, Japanese cedar pollen, grass pollens, ragweed and house dust mite clinical trials have shown safety, efficacy and tolerability to PIT. Hence, PIT may hold the potential to change the treatment algorithm for allergic rhinitis.
The prevalence of cat allergen-induced AR is increasing worldwide, prompting its study using controlled methodology. Three general categories of allergen exposure models currently exist for the study of cat allergen-induced AR: natural exposure cat rooms, allergen exposure chambers (AEC), and nasal allergen challenges (NAC). We evaluated existing literature surrounding the use of these models to study cat allergen induced AR using online research databases, including OVID Medline, Embase, and Web of Science. We report that natural exposure cat rooms have been important in establishing the foundation for our understanding of cat allergen-induced AR. Major limitations, including variable allergen ranges and differing study designs highlight the need for a more standardized protocol. In comparison, AECs are an exceptional model to mimic real-world allergen exposure and study long-term implications of AR with large sample sizes. Existing AECs are limited by heterogeneous facility designs, differing methods of cat allergen distribution, and issues surrounding cost and accessibility. Conversely, NACs allow for smaller participant cohorts for easier biological sampling and are ideal for phase I, phase 2 or proof-of-concept studies. NACs generally have a standardized protocol and are less expensive compared to AECs. Nevertheless, NACs solely capture acute allergen exposure and have the further limitation of using allergen extracts rather than natural allergen. As the use of combined controlled methodologies is sparse, we recommend concurrent use of AECs and NACs to study short- and long-term effects of AR, thereby providing a more holistic representation of cat allergen-induced AR.
Investigation of immediate hypersensitivity has been hampered by the limitations of using polyclonal IgE ab, present at low concentrations in allergic sera. Our goal was to isolate human monoclonal IgE antibodies (mAb) to specific allergens as they occur in vivo, to evaluate their allergen specificity, potency and binding activity. METHODS: Human IgE mAb (n520) were obtained by electrical cytofusion of cultured human B cells from peripheral blood of allergic patients. IgE mAb were quantified by ImmunoCAP and analyzed by SDS-PAGE. IgE mAb dose response curves to major inhalant and food allergens (e.g. Der p 1, Fel d 1, Ara h 2, Gal d 2) were compared by ELISA. RESULTS: IgE mAb were produced in mg amounts (1mg IgE is ;416,000 IU) and targeted major inhaled allergens (e.g. mite, dog, and cat) and foods (peanut, cashew, walnut, milk, and egg). IgE mAb directed against different epitopes were obtained (e.g. to Der p 2). ELISA dose response curves were sigmoidal with limits of detection of <1ng/ml, indicating the IgE mAb had high affinity. CONCLUSIONS: Natural human IgE mAb to a diverse panel of clinically important allergens are unique probes for allergen identification, quantification of IgE antibody responses, epitope analysis and mast cell and basophil activation assays. Human IgE mAb used as calibrators will improve in vitro allergy molecular diagnostics and reduce dependence on allergic sera. They will also enable mechanistic studies of IgE mediated allergic reactions.
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