Studies on specific immune diseases elucidate how disrupted chemical transport mechanisms contribute to disease pathology. In asthma, the overproduction of mucus and increased vascular permeability result from dysregulated cytokine and chemokine signaling, leading to airway obstruction and compromised respiratory mechanics. Such findings underscore the need for targeting these transport pathways in therapeutic approaches . For allergic reactions, chemotaxis and adhesion molecule regulation are disrupted, causing inappropriate immune cell accumulation and tissue damage. This leads to compromised biomechanical properties of respiratory tissues, manifesting as asthma with its characteristic airway hyper-responsiveness . Thus, allergy pathogenesis is marked by specific biophysical and biomechanical disruptions. Upon allergen exposure, the release of histamine and other mediators increases vascular permeability, causing edema and tissue swelling . The chemoattraction of immune cells like eosinophils to the site via chemotactic gradients exacerbates inflammation, leading to chronic tissue remodeling and altered biomechanics . Figure presents a schematic flow process that can guide the modeling framework for allergenicity. It systematically shows the mechanisms underlining and guiding the interstitial tissue and vascular events. These events are captured under two major phases, the sensitization and effector phases (Figure ). The sensitization phase of allergic airway sensitization involves allergen sources, dendritic cells (DC) transforming into antigen-presenting cells (APCs), activation of naive T cells in the lymph node, and cytokine secretion by activated T cells. The other aspect of the sensitization phase is B cell differentiation, which involves B cell activation, proliferation, and differentiation. The effector phase consists of an early phase (IgE binding to mast cells, reexposure, and degranulation) and a late phase (cell death, vasopermeability, endothelial retraction, and bronchoconstriction). Despite advances, significant knowledge gaps remain regarding the precise regulation of species transport and transformation in immune diseases. Further research is needed to elucidate the spatiotemporal dynamics of these processes and their precise roles in disease progression and response to treatment. Understanding these aspects can lead to more effective and less invasive therapeutic interventions. Chemical species transport and transformation play crucial roles in the pathophysiological conditions of the immune system. From localized chemical gradients driving cell migration to bulk flow facilitating systemic immune surveillance, these processes are integral to immune homeostasis and pathology. The complex interplay between these mechanisms underscores the importance of integrating biophysical and biochemical insights into disease diagnosis and treatment strategies. For allergic diseases, specifically, interventions targeting these transport mechanisms hold promising potential to restore tissue stability and function. Additionally, a deeper understanding of the roles of species transport and transformation during sensitization process to allergens is crucial for preventing the onset of allergic diseases. Further research into these dynamic processes will bridge existing knowledge gaps and enhance therapeutic outcomes.