Abstract
The pathophysiology of immunoglobulin E (IgE) mediated food allergy has been understood on a superficial level for several decades. Surveillance by dendritic cells for exogenous antigens leads to a high-affinity IgE response that arms effector cells (sensitization), such that subsequent exposures can trigger a type 1 hypersensitivity recall response. However, merely scratching the surface, whether confronting unmet needs in a clinical setting or probing the basic immunology of allergic immunity, quickly reveals the many unmet fundamental questions that lie there. This review article focused on the following such questions. Why are common allergens common? How does sensitization most often occur? How is IgE maintained over long time periods, even in the apparent absence of exposure? What distinguishes sensitization from clinical allergy? Can we stratify risk (i.e., sensitivity and severity)? What distinguishes the pathophysiology of non-IgE-mediated allergy when so much of it seems to overlap?