In the immune system, dysfunctions in the immune response resulting in tissue injury and disease are classified as hypersensitivity reactions. Among these, Type I hypersensitivity reactions, also widely known as allergic or atopic reactions, occur when the body wrongly identifies a typically non-dangerous substance (allergen) as a threat. This process begins in a phase dubbed prior sensitization, where an antigen-presenting cell presents the allergen to a CD4+ T cell. This cell differentiates into a Th2 cell and begins to secrete IL-4.
IL-4 instructs B-cells to class switch and transform into IgE. Changes in the environment, such as the introduction of pollen, trigger these IgE molecules to identify and become sensitized to the allergen. Upon repeat contact with the allergen, the body reacts in two phases√ê the immediate phase and the delayed phase. During the immediate phase, circulating IgE activate mast cells and basophils, mast cells and basophils, causing them to degranulate and produce an allergic reaction. Concurrently, Th2 cells secrete IL-5, which activates eosinophils from the bone marrow that then travel to the allergen site. This process, which may take hours, is the delayed phase of the reaction.
High levels of eosinophils notably contribute to the symptoms observed in asthma, allergic rhinitis, and dermatitis. Examples of Type I hypersensitivity reactions include anaphylaxis, drug allergies such as a penicillin allergy, food allergies like those to nuts and shellfish, and environmental allergies, such as allergies to dust mites, pollen, and latex.
A Type I Hypersensitivity Reaction is an abnormal immune response characterized by the production of specific IgE antibodies in response to an allergen. These reactions lead to various allergic symptoms, such as those seen in allergic rhinitis, asthma, and dermatitis, and are based on the area of the body where the reaction occurs and the nature of the allergen.
During a Type I Hypersensitivity reaction, the antigen presenting cell (often a dendritic cell) captures the allergen and presents it to a CD4+ T cell, which differentiates into a Th2 cell. It then produces a cytokine known as Interleukin 4 (IL-4). IL-4 triggers B cells to produce IgE antibodies specific to the allergen. Upon repeat exposure to the allergen, IgE activates mast cells and basophils, causing them to degranulate and produce an immediate allergic reaction. Concurrently, Th2 cells also secrete IL-5, which activates eosinophils from the bone marrow that then travel to the allergen site. This process, which may take hours, is the delayed phase of the reaction.
Basophils and mast cells play a crucial role in Type I hypersensitivity reactions. When an allergen enters the body, the IgE antibodies become sensitized to recognize that particular allergen. Upon second exposure to the same allergen, IgE activates mast cells and basophils, which rapidly degranulate, releasing a variety of substances, such as histamine, that promote inflammation and other allergic symptoms.
Eosinophils are a type of white blood cell that are active during a Type I hypersensitivity reaction. Th2 cells secrete IL-5, which activates eosinophils from the bone marrow that then travel to the allergen site. This process, which may take hours, is the delayed phase of the reaction. Once at the site of the allergic reaction, eosinophils release substances that further enhance the immune response, contributing to tissue damage and inflammation that characterize allergic reactions.
Anaphylaxis is a severe, life-threatening allergic reaction that can occur in Type I hypersensitivity. When the body is exposed to an allergen it has been sensitized to, the immune system triggers a widespread release of inflammatory mediators from mast cells and basophils. If this release is systemic, it can cause whole-body symptoms such as difficulty breathing, a drop in blood pressure, and loss of consciousness. This severe response is known as anaphylaxis and it requires immediate medical attention.