ABAI key terms

A personal or family tendency to become sensitized and produce IgE antibodies against common environmental allergens, predisposing to asthma, allergic rhinitis, and eczema.

Any normally harmless environmental protein that triggers an IgE-mediated immune response in a susceptible person, such as pollen, dust mite, or food proteins.

The initial development of allergen-specific IgE after exposure, which primes mast cells and basophils but does not by itself produce clinical symptoms on re-exposure.

An immediate allergic reaction caused by allergen cross-linking of IgE on mast cells, releasing histamine and other mediators within minutes of exposure.

A tissue-resident immune cell bearing high-affinity IgE receptors that degranulates on allergen cross-linking, releasing histamine, tryptase, and lipid mediators.

A protease stored in mast cell granules and released during degranulation; elevated serum levels support a diagnosis of anaphylaxis, especially when sampled soon after onset.

A biogenic amine released from mast cells and basophils that causes vasodilation, vascular leak, bronchoconstriction, itching, and mucus secretion in allergic reactions.

A severe, rapidly developing systemic hypersensitivity reaction involving airway, breathing, or circulation compromise, treated promptly with intramuscular epinephrine.

The first-line drug for anaphylaxis; alpha-adrenergic effects reverse vasodilation and edema while beta effects relax bronchial smooth muscle and blunt mediator release.

Raised, itchy, erythematous wheals caused by superficial dermal edema from mast cell mediator release; individual lesions typically resolve within 24 hours.

Deeper swelling of the dermis and subcutaneous or submucosal tissue, often of lips, eyelids, or airway, which may be histamine-mediated or bradykinin-mediated.

An autosomal dominant disorder of C1 inhibitor deficiency or dysfunction causing recurrent bradykinin-driven swelling without urticaria, unresponsive to antihistamines or epinephrine.

A serine protease inhibitor that restrains complement and contact-pathway activation; its deficiency permits excess bradykinin generation and episodic angioedema.

IgE-mediated inflammation of the nasal mucosa producing sneezing, rhinorrhea, itching, and congestion, often seasonal or perennial and frequently accompanying asthma.

Repeated administration of allergen by subcutaneous or sublingual routes to induce immune tolerance, reducing symptoms and modifying the natural course of allergic disease.

A bedside test in which allergen extracts are pricked into the epidermis; a wheal-and-flare response within about 15 minutes indicates allergen-specific IgE.

Antibody directed against a particular allergen, measured in serum by immunoassay to help confirm sensitization when skin testing is unsafe or unreliable.

The antibody class that binds high-affinity receptors on mast cells and basophils and mediates immediate allergic reactions; present at very low serum concentrations.

A granulocyte with eosin-staining granules that releases cytotoxic proteins and cytokines, prominent in allergic inflammation, asthma, and parasitic defense.

An elevated number of eosinophils in blood or tissue, which may reflect allergy, drug reaction, parasitic infection, or a primary hypereosinophilic disorder.

An immune pattern driven by T helper 2 cells and innate lymphoid cells, with IL-4, IL-5, and IL-13 promoting IgE, eosinophilia, mucus, and airway hyperresponsiveness.

A cytokine that drives eosinophil growth, activation, and survival; it is the target of biologic therapies used in severe eosinophilic asthma.

A CD4 T cell subset that secretes IL-4, IL-5, and IL-13, supporting IgE class switching and eosinophilic inflammation characteristic of allergic disease.

An inherited defect in one or more components of the immune system, presenting with recurrent, severe, or unusual infections, autoimmunity, or malignancy.

A heterogeneous primary antibody deficiency causing low immunoglobulins and poor vaccine responses, with recurrent sinopulmonary infections and increased autoimmunity risk.

A group of inherited disorders with profound T cell defects, presenting in infancy with severe infections and requiring hematopoietic stem cell transplantation or gene therapy.

Population testing of infants, including measurement of T cell receptor excision circles, to detect severe combined immunodeficiency before infections become life-threatening.

Pooled human antibody given intravenously or subcutaneously to patients with antibody deficiency to prevent infections and reduce complications.

A cascade of plasma proteins that opsonizes microbes, lyses cells via the membrane attack complex, and amplifies inflammation and immune clearance.

A cell such as a neutrophil or macrophage that engulfs and destroys microbes; defects in phagocyte number or function cause recurrent bacterial and fungal infections.

An abnormally low blood neutrophil count that raises susceptibility to bacterial and fungal infection, often caused by drugs, marrow disease, or immune destruction.

An adaptive immune response directed against the body's own tissues, arising when self-tolerance fails and producing organ-specific or systemic inflammatory disease.

An antibody that binds a self antigen; some directly cause disease by stimulating, blocking, or destroying target cells, while others serve mainly as diagnostic markers.

Deletion or functional inactivation of self-reactive lymphocytes during their development in the thymus or bone marrow, preventing autoimmunity.

A CD4 T cell subset, marked by FOXP3, that suppresses self-reactive and excessive immune responses; its deficiency causes severe multi-organ autoimmunity.

A set of highly polymorphic cell-surface molecules that present peptide antigens to T cells and determine tissue compatibility in transplantation.

The antigen-recognition receptor on T lymphocytes that binds peptide displayed by major histocompatibility complex molecules and triggers T cell activation.

Donor T cells in a transplant recognize recipient tissues as foreign and attack them, causing skin, gut, and liver injury, most often after stem cell transplantation.

Temporary induction of tolerance by rapidly escalating drug doses, allowing a patient with prior hypersensitivity to receive an essential medication safely.