α-Gal syndrome is characterized by specific IgE (sIgE) antibodies to the carbohydrate galactose-α-1,3-galactose (α-Gal) and delayed onset of allergic symptoms after ingestion of mammalian meat. While tick bites are assumed to mediate sensitization, the immune response to tick bites has not yet been investigated. To investigate the peripheral immune response to tick bites in humans over time.

De novo food allergy is a common phenomenon among pediatric solid organ recipients (8.5%-57%) when compared with the general population (0.45%-10%). Other associated disorders include non-IgE-mediated immune reactions and clinical predisposition to asthma and alterations in the oral mucosa. Originally, passive mechanisms (passive transfer of IgE and immune cells) were thought to be responsible for acute, transient cases of food allergies with a previous history of sensitization for a specific allergen in the donor. Recently proposed pathophysiological mechanisms to explain de novo allergies include TH2/B-cell imbalance, regulatory T-cell (Treg) disruption, gastrointestinal immaturity, and altered gastrointestinal permeability. Recent studies also suggest that immunosuppressive drugs, especially tacrolimus, promote naïve T-cell differentiation into TH2 cells, IgE-promoting cytokine production, decreased IL-5 and IL-10 levels, increased IgA levels, and Treg disruption. Such immunological interactions, in conjunction with altered intestinal permeability, intestinal immaturity in children, history of viral infection, and a personal history of allergies or eczema, are thought to explain most clinical cases of pediatric de novo food allergy after solid organ transplantation reported in the literature. A better understanding of the immunological mechanisms underpinning organ donors and recipients may unveil some of the caveats concerning therapeutic management and improve the quality of life of affected individuals.

Asthma, a prevalent chronic respiratory disease, manifests in heterogeneous phenotypes and endotypes, necessitating bespoke therapeutic approaches. Asthma exacerbations are characterized by worsening of symptoms and decline in lung function and present substantial challenges despite advances in understanding and treatment. Viral respiratory infections, notably those caused by rhinovirus, serve as primary triggers, with allergic sensitization and environmental exposures increasing susceptibility. Deficient antiviral responses in asthmatic airway epithelial cells, particularly impaired interferon production, perpetuate inflammation and hyperresponsiveness, contributing to exacerbations. Additionally, genetic polymorphisms influence host responses and susceptibility. Recent studies underscore the association between specific inflammatory profiles, particularly eosinophil-mediated inflammation, and the frequency of exacerbations. Biologic therapies targeting inflammatory pathways show promise in reducing the frequency of exacerbations, thus underscoring the importance of understanding inflammatory phenotypes when selecting treatment. Notably, T2 inhibitors may modulate immune responses, potentially mitigating viral exacerbations. Characterizing exacerbations is crucial for optimizing therapeutic strategies. Evidence suggests a dissociation between baseline inflammatory profiles and exacerbation phenotypes, highlighting the need for individualized management. Phenotyping exacerbations using sputum analysis helps to identify predominant inflammatory patterns and thus inform treatment decisions. The varied responses to biologic therapies further emphasize the importance of phenotyping exacerbations in refining treatment algorithms. In conclusion, phenotyping asthma exacerbations provides valuable insights into underlying inflammatory mechanisms and enables personalized therapy. Understanding the complex interplay between viral triggers, inflammatory pathways, and responses to treatment is essential if we are to effectively manage severe asthma and reduce the burden of exacerbations. Further research into the mechanistic actions of biologic therapies in mitigating viral exacerbations is warranted to optimize asthma management strategies.